A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Tumors or cancer of the PROSTATE.
A gland in males that surrounds the neck of the URINARY BLADDER and the URETHRA. It secretes a substance that liquefies coagulated semen. It is situated in the pelvic cavity behind the lower part of the PUBIC SYMPHYSIS, above the deep layer of the triangular ligament, and rests upon the RECTUM.
A cell line derived from cultured tumor cells.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
A glycoprotein that is a kallikrein-like serine proteinase and an esterase, produced by epithelial cells of both normal and malignant prostate tissue. It is an important marker for the diagnosis of prostate cancer.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is PROTO-ONCOGENE PROTEINS C-MET.
Cell surface protein-tyrosine kinase receptors for HEPATOCYTE GROWTH FACTOR. They consist of an extracellular alpha chain which is disulfide-linked to the transmembrane beta chain. The cytoplasmic portion contains the catalytic domain and sites critical for the regulation of kinase activity. Mutations of the gene for PROTO-ONCOGENE PROTEINS C-MET are associated with papillary renal carcinoma and other neoplasia.
A cell surface receptor involved in regulation of cell growth and differentiation. It is specific for EPIDERMAL GROWTH FACTOR and EGF-related peptides including TRANSFORMING GROWTH FACTOR ALPHA; AMPHIREGULIN; and HEPARIN-BINDING EGF-LIKE GROWTH FACTOR. The binding of ligand to the receptor causes activation of its intrinsic tyrosine kinase activity and rapid internalization of the receptor-ligand complex into the cell.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).
An abnormal protein with unusual thermosolubility characteristics that is found in the urine of patients with MULTIPLE MYELOMA.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Cis-acting DNA sequences which can increase transcription of genes. Enhancers can usually function in either orientation and at various distances from a promoter.
Software used to locate data or information stored in machine-readable form locally or at a distance such as an INTERNET site.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis. (1/724)

Here we report that in staurosporine-induced apoptosis of HeLa cells, Bid, a BH3 domain containing protein, translocates from the cytosol to mitochondria. This event is associated with a change in conformation of Bax which leads to the unmasking of its NH2-terminal domain and is accompanied by the release of cytochrome c from mitochondria. A similar finding is reported for cerebellar granule cells undergoing apoptosis induced by serum and potassium deprivation. The Bax-conformational change is prevented by Bcl-2 and Bcl-xL but not by caspase inhibitors. Using isolated mitochondria and various BH3 mutants of Bid, we demonstrate that direct binding of Bid to Bax is a prerequisite for Bax structural change and cytochrome c release. Bcl-xL can inhibit the effect of Bid by interacting directly with Bax. Moreover, using mitochondria from Bax-deficient tumor cell lines, we show that Bid- induced release of cytochrome c is negligible when Bid is added alone, but dramatically increased when Bid and Bax are added together. Taken together, our results suggest that, during certain types of apoptosis, Bid translocates to mitochondria and binds to Bax, leading to a change in conformation of Bax and to cytochrome c release from mitochondria.  (+info)

Solution structure of BID, an intracellular amplifier of apoptotic signaling. (2/724)

We report the solution structure of BID, an intracellular cross-talk agent that can amplify FAS/TNF apoptotic signal through the mitochondria death pathway after Caspase 8 cleavage. BID contains eight alpha helices where two central hydrophobic helices are surrounded by six amphipathic ones. The fold resembles poreforming bacterial toxins and shows similarity to BCL-XL although sequence homology to BCL-XL is limited to the 16-residue BH3 domain. Furthermore, we modeled a complex of BCL-XL and BID by aligning the BID and BAK BH3 motifs in the known BCL-XL-BAK BH3 complex. Additionally, we show that the overall structure of BID is preserved after cleavage by Caspase 8. We propose that BID has both BH3 domain-dependent and -independent modes of action in inducing mitochondrial damage.  (+info)

Solution structure of the proapoptotic molecule BID: a structural basis for apoptotic agonists and antagonists. (3/724)

Members of the BCL2 family of proteins are key regulators of programmed cell death, acting either as apoptotic agonists or antagonists. Here we describe the solution structure of BID, presenting the structure of a proapoptotic BCL2 family member. An analysis of sequence/structure of BCL2 family members allows us to define a structural superfamily, which has implications for general mechanisms for regulating proapoptotic activity. It appears two criteria must be met for proapoptotic function within the BCL2 family: targeting of molecules to intracellular membranes, and exposure of the BH3 death domain. BID's activity is regulated by a Caspase 8-mediated cleavage event, exposing the BH3 domain and significantly changing the surface charge and hydrophobicity, resulting in a change of cellular localization.  (+info)

Caspases induce cytochrome c release from mitochondria by activating cytosolic factors. (4/724)

We investigated the ability of caspases (cysteine proteases with aspartic acid specificity) to induce cytochrome c release from mitochondria. When Jurkat cells were induced to undergo apoptosis by Fas receptor ligation, cytochrome c was released from mitochondria, an event that was prevented by the caspase inhibitor, zVAD-fmk (zVal-Ala-Asp-CH2F). Purified caspase-8 triggered rapid cytochrome c release from isolated mitochondria in vitro. The effect was indirect, as the presence of cytosol was required, suggesting that caspase-8 cleaves and activates a cytosolic substrate, which in turn is able to induce cytochrome c release from mitochondria. The cytochrome c releasing activity was not blocked by caspase inhibition, but was antagonized by Bcl-2 or Bcl-xL. Caspase-8 and caspase-3 cleaved Bid, a proapoptotic Bcl-2 family member, which gains cytochrome c releasing activity in response to caspase cleavage. However, caspase-6 and caspase-7 did not cleave Bid, although they initiated cytochrome c release from mitochondria in the presence of cytosol. Thus, effector caspases may cleave and activate another cytosolic substrate (other than Bid), which then promotes cytochrome c release from mitochondria. Mitochondria significantly amplified the caspase-8 initiated DEVD-specific cleavage activity. Our data suggest that cytochrome c release, initiated by the action of caspases on a cytosolic substrates, may act to amplify a caspase cascade during apoptosis.  (+info)

Ion channel activity of the BH3 only Bcl-2 family member, BID. (5/724)

BID is a member of the BH3-only subgroup of Bcl-2 family proteins that displays pro-apoptotic activity. The NH(2)-terminal region of BID contains a caspase-8 (Casp-8) cleavage site and the cleaved form of BID translocates to mitochondrial membranes where it is a potent inducer of cytochrome c release. Secondary structure and fold predictions suggest that BID has a high degree of alpha-helical content and structural similarity to Bcl-X(L), which itself is highly similar to bacterial pore-forming toxins. Moreover, circular dichroism analysis confirmed a high alpha-helical content of BID. Amino-terminal truncated BIDDelta1-55, mimicking the Casp-8-cleaved molecule, formed channels in planar bilayers at neutral pH and in liposomes at acidic pH. In contrast, full-length BID displayed channel activity only at nonphysiological pH 4.0 (but not at neutral pH) in planar bilayers and failed to form channels in liposomes even under acidic conditions. On a single channel level, BIDDelta1-55 channels were voltage-gated and exhibited multiconductance behavior at neutral pH. When full-length BID was cleaved by Casp-8, it too demonstrated channel activity similar to that seen with BIDDelta1-55. Thus, BID appears to share structural and functional similarity with other Bcl-2 family proteins known to have channel-forming activity, but its activity exhibits a novel form of activation: proteolytic cleavage.  (+info)

A novel BH3-like domain in BID is required for intramolecular interaction and autoinhibition of pro-apoptotic activity. (6/724)

Upon activation of the Fas apoptotic signaling pathway, Bid, a "BH3 domain-only" pro-apoptotic molecule, is cleaved by caspase-8 into a 6.5-kDa N-terminal and a 15-kDa BH3 domain-containing C-terminal fragment, referred to as t(n)-Bid and t(c)-Bid, respectively. t(c)-Bid is a more potent inducer of apoptosis than full-length Bid, suggesting that the N-terminal region of Bid has an inhibitory effect on its pro-apoptotic activity. Here, we report the identification of a novel BH3-like motif (amino acid residues 35-43) in t(n)-Bid. Although Bid does not homodimerize, t(n)-Bid is able to associate avidly with t(c)-Bid. Site-directed mutagenesis revealed that both the novel BH3-like and BH3 domains are necessary for direct binding between t(n)-Bid and t(c)-Bid. While full-length Bid does not associate with t(n)-Bid, substitution of Leu(35), a critical residue in mediating t(n)-Bid/t(c)-Bid interaction, with Ala in full-length Bid is sufficient to establish Bid/t(n)-Bid interaction. Interestingly, the L35A Bid mutant is as effective as t(c)-Bid in inducing apoptosis and binding Bcl-X(L). We propose that the intramolecular interaction involving the BH3-like and BH3 domains serves to regulate the pro-apoptotic potential of Bid.  (+info)

The tyrosine kinase lck is required for CD95-independent caspase-8 activation and apoptosis in response to ionizing radiation. (7/724)

Induction of apoptosis is a hallmark of cytostatic drug and radiation-induced cell death in human lymphocytes and lymphoma cells. However, the mechanisms leading to apoptosis are not well understood. We provide evidence that ionizing radiation induces a rapid activation of caspase-8 (FLICE) followed by apoptosis independently of CD95 ligand/receptor interaction. The radiation induced cleavage pattern of procaspase-8 into mature caspase-8 resembled that following CD95 crosslinking and resulted in cleavage of the proapoptotic substrate BID. Overexpression of dominant-negative caspase-8 interfered with radiation-induced apoptosis. Caspase-8 activation by ionizing radiation was not observed in cells genetically defective for the Src-like tyrosine kinase Lck. Cells lacking Lck also displayed a marked resistance towards apoptosis induction upon ionizing radiation. After retransfection of Lck, caspase-8 activation and the capability to undergo apoptosis in response to ionizing radiation was restored. We conclude that radiation activates caspase-8 via an Lck-controlled pathway independently of CD95 ligand expression. This is a novel signaling event required for radiation induced apoptosis in T lymphoma cells.  (+info)

Evidence for a function of death-receptor-related, death-domain-containing proteins in anoikis. (8/724)

Normal epithelial cells undergo apoptosis if integrinmediated matrix contacts are lost, in a process termed 'anoikis'. Anoikis prevents shed epithelial cells from colonizing elsewhere, and is thus essential for maintaining appropriate tissue organisation. Aberrant oncogenes or tumor suppressor genes can cause resistance to anoikis, thereby contributing substantially to malignancy. Apoptosis is mediated by a well-ordered signaling cascade, which involves activation of intracellular proteases known as caspases. However, the mechanism by which the caspase cascade is initiated following cell-matrix detachment is unknown. We have hypothesized that death receptor activation might be involved in anoikis. To test this hypothesis, we developed a transient assay for anoikis and used it to assay the effects of proteins that block the function of domains found within death receptors known as death domains. In this assay, silencer of death domains (SODD) and dominant-negative FAS-associated death domain protein (FADD) efficiently inhibited anoikis in Madin-Darby canine kidney (MDCK) cells. The protective activity of SODD required its BAG domain, which interacts with the heat shock proteins hsp70 and hsc70, and inhibits the chaperone activity of the latter. Both caspase 8, which physically associates with death receptors, and cleavage of the caspase-8 substrate BID, were activated by cell-matrix detachment. These findings indicate a role for death receptors or proteins with related death domains in triggering anoikis.  (+info)

Chemical-registry-number] 0 / Antigens, CD95; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Carrier Proteins; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / ...
The mitochondrial carrier homologue-2 (MTCH2). Binds the BH3-interacting domain death agonist, BID. Regulated (induced) by the hepatocyte growth factor receptor, HGF/SF or Met. It has been proposed that its transport function has been lost (Robinson et al., 2012). Surprisingly, this protein has been reported to be targetted to the outer mitochondrial membrane (Gutiérrez-Aguilar and Baines, 2013 ...
Bid antibody (BH3 interacting domain death agonist) for ELISA, ICC/IF, IHC-P, WB. Anti-Bid pAb (GTX31689) is tested in Mouse samples. 100% Ab-Assurance.
Background The fundamental oil (EO) of L. particular caspase inhibitors showed that activation of caspase-8 was following and reliant towards the activation of caspases-9 and -3. In addition, the fundamental essential oil triggered a disruption from the mitochondrial transmembrane potential (m), improved the discharge of cytochrome towards the cytosol, and modified the manifestation of certain people of Bcl-2 family members (Bcl-2, Bax and Bet), Apaf-1 and XIAP. Oddly enough, low dosages of AVO-b and AVO-1 induced apoptosis in a variety of malignancy cellular lines also, however, not in noncancerous cellular material. Conclusions The full total outcomes demonstrate how the EO-induced apoptosis in HL-60 cellular material is definitely mediated by caspase-dependent pathways, concerning caspases-3, -9, and -8, that are initiated by Bcl-2/Bax/Bid-dependent lack of 173039-10-6 manufacture m resulting in launch of cytochrome towards the cytoplasm to activate the caspase cascade. The discovering that ...
Background The fundamental oil (EO) of L. particular caspase inhibitors showed that activation of caspase-8 was following and reliant towards the activation of caspases-9 and -3. In addition, the fundamental essential oil triggered a disruption from the mitochondrial transmembrane potential (m), improved the discharge of cytochrome towards the cytosol, and modified the manifestation of certain people of Bcl-2 family members (Bcl-2, Bax and Bet), Apaf-1 and XIAP. Oddly enough, low dosages of AVO-b and AVO-1 induced apoptosis in a variety of malignancy cellular lines also, however, not in noncancerous cellular material. Conclusions The full total outcomes demonstrate how the EO-induced apoptosis in HL-60 cellular material is definitely mediated by caspase-dependent pathways, concerning caspases-3, -9, and -8, that are initiated by Bcl-2/Bax/Bid-dependent lack of 173039-10-6 manufacture m resulting in launch of cytochrome towards the cytoplasm to activate the caspase cascade. The discovering that ...
MOHA Bids Are invited forRefined Oil IS 11069 Soybean oil Black Tea IS 3633 Roasted Almonds Kismis Raisins Total Quantity 3854 , Due Date: 21-06-2021 ,Tender Value: 0 , Location: Uttaranchal Tender Notice 28140320
Latest Online Govt Tenders of Telangana Administration, invitation to bid expression of interest, Online Port Blair Tender Notice Notification, e-Tender, e-Procurement, Travel Tourism Tenders
PHP & tietojärjestelmäarkkitehtuuri Projects for $100. We are looking for someone to secure our backend control panel from SQL injection. Our system is built using PHP and OOP. Please only bid if you have extensive knowledge in PHP and OOP. We will have...
INTERNAL CANDIDATES: Please submit your bid by clicking on the APPLY button no later than 12:00 Noon, on the closing date. Complete ALL fields on the electronic bid form. Failure to complete the job bid may render you ineligible for this position. Please direct all questions to Human Resources: 814.234.6143. ...
Bid procedure, 2021-07-06BondsKOMMUNINVEST I SVERIGE: 2505. SE0011414010. 2025-05-12KOMMUNINVEST I SVERIGE: 2611, SE0012569572, 2026-11-12KOMMUNINVEST I SVERIGE: 2805, SE0015660139, 2028-05-12 BidsBids on interest and volume are entered via Bloomberg Bond Auction SystemBid date2021-07-06Bid times10.00-11.00 (CET/CEST) on the Bid dateRequested volume (corresponding nominal amount)2505: 500 mln SEK +/-250 mln SEK2611: 750 mln SEK +/-400 mln SEK2805: 750 mln SEK +/-400 mln SEK Highest permitted bid
Government Bid Opportunity: Z--Telecommunications cable, infrastructure installation. Access many more Z - Maintenance, Repair or Alteration of Real Property Bids | Get your Free Government Bids Alert!
A bid given to the balancing power market to increase generation or reduce consumption. When the bid is activated, the party carrying out the regulation sells regulating power to Fingrid.. ...
Government Pre-Bid Opportunity: K--Cadmium Plating. Access many more K - Modification of Equipment Upcoming Bids | Get your Free Government Bids Alert!
Hewitt Associates agreed to acquire Exult for about $691 million in stock, in a bid to expand its presence in the business-process-outsourcing market.
A blog about herpetology: snakes, lizards, frogs, salamanders, turtles, ecology, evolution, behavior, conservation, recent research, phylogeny.
Looking for online definition of apoptic death agonist in the Medical Dictionary? apoptic death agonist explanation free. What is apoptic death agonist? Meaning of apoptic death agonist medical term. What does apoptic death agonist mean?
Two types of cell death can be distinguished by morphological features, although it is likely that these are two ends of a spectrum with possible intermediate forms. Apoptosis involves shrinkage, nuclear disassembly, and fragmentation of the cell into discrete bodies with intact plasma membranes. These are rapidly phagocytosed by neighbouring cells. An important feature of apoptosis is the requirement for adenosine triphosphate (ATP) to initiate the execution phase. In contrast, necrotic cell death is characterized by cell swelling and lysis. This is usually a consequence of profound loss of mitochondrial function and resultant ATP depletion, leading to loss of ion homeostasis, including volume regulation, and increased Ca2+. The latter activates a number of nonspecific hydrolases (i.e., proteases, nucleases, and phospholipases) as well as calcium dependent kinases. Activation of calpain I, the Ca2+-dependent cysteine protease cleaves the death-promoting Bcl-2 family members Bid and Bax which ...
The board may issue and sell the bonds of the district at not less than par value, and the proceeds shall be placed in the treasury of the county. Before selling the bonds, or any part thereof, the legislative body shall give notice not less than 10 days prior to the date of sale by publication pursuant to Section 6061 of the Government Code in a newspaper of general circulation circulating in the district inviting sealed bids in such manner as the legislative body shall prescribe. If satisfactory bids are received, the bonds offered for sale shall be awarded to the highest responsible bidder. If no bids are received, or if the legislative body determines that the bids received are not satisfactory as to price or responsibility of the bidders, the legislative body may reject all bids received, if any, and either readvertise or sell the bonds at private sale.. All premiums and accrued interest received shall be paid into the fund to be used for the payment of principal and interest on the bonds ...
For having zero national title implications, Week 15 in the Big 12 is about as exciting as it can get. Three teams will have a chance to win the conference: Baylor, Oklahoma State and Texas...
Mail-In Bids The NI Mail Bid Sale is offered twice per year. Although these lots can be viewed by the general public, offers and bids are only accepted from NI members. Click to learn more about terms of sale. ...
Our annual calf pasture bid sale is in September. Bids are due by 6 p.m. on Sunday, September 27. Most calves are base priced at $1500.. ...
Ethiopia. 5. Bidders should submit their offers accompanied by copies of all appropriate documents/license in a wax-sealed and stamped envelope to the above address into the box ready for the bid before 4:30 P.M. on April 28, 2006.. 6. Bidders shall furnish as part of their bid, bid security the amount of ETB 10,000 (Ten Thousand Birr) in the form of certified cheque (CPO) issued by a recognized bank, which will be refunded as soon as the first stock of production is received by GOAL Ethiopia as per the specification.. 7. Bid will be opened in the presence of bidders, their legal representatives who choose to attend on May 2, 2006 at 9:00 A.M. at the GOAL Ethiopia s meeting Room, Head Office, Addis Ababa.. 8. GOAL Ethiopia receives the right to accept or reject any or all bids.. GOAL Ethiopia ...
If offering a product or service, please compete the following form. Technology Department staff will consult submissions and contact vendors when pricing and bids are needed for appropriate products and services indicated ...
2010 MITSUBISHI ENDEAVOR The Mitsubishi Endeavor is a middle-bundle crossing fomite, has few human opinion, nearly as large Outlander file, change the address, and bids are inaugurating the third row, who tried not to. Afterwards.... ...
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Rumis Masnavi - O body with thy hundred (worldly) concerns, bid me farewell: thou hast taken my life: (now) seek another (victim).
Klavunat Bid; zat rree, kulakta geli en enfeksiyonlar, bron it, sin zit, idrar yollar iltihab ve cilt enfeksiyonlar n n tedavisinde etkilidir.
When it pertains to deciding between a new build in Shalstone or an existing home there are advantages and also disadvantages with both. You need to weigh up
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Sony said years ago that it was targeting the #1 spot among camera manufacturers, and yesterday we learned that despite mixed success in the quest so far, the company is still deadly serious about that longtime goal. The new Sony...
The current bid and offer are $74.00 and $80.00, respectively. If you think the index will be above $3,784 at 11 a.m., you buy the binary option at $80, or place a bid at a lower price and hope ...
Sony said years ago that it was targeting the #1 spot among camera manufacturers, and yesterday we learned that despite mixed success in the quest so far, the company is still deadly serious about that longtime goal. The new Sony...
以前我一直在買專櫃的衣服,認為要現場挑衣服才有保障,不太敢在網路上買衣服,因為害怕收到貨時與圖色差太大,或是怕…
Critical issues in apoptosis include the importance of caspases versus organelle dysfunction, dominance of anti- versus proapoptotic BCL-2 members, and whether commitment occurs upstream or downstream of mitochondria. Here, we show cells deficient for the downstream effectors Apaf-1, Caspase-9, or C …
Head and neck squamous cell carcinomas (HNSCC) induced by human papilloma virus (HPV) have increased recently in the US, and exhibit a different prognosis and response to therapies from HPV(-) cancers. Analysis of HNSCC TCGA datasets provide evidence for distinct alterations in expression of components of the NF-κB and death pathways in HNSCC with different HPV status. Previously, we have found that birinipant, a novel SMAC mimetic that inhibits inhibitor of apoptosis proteins (IAPs), sensitizes a subset of HPV(-) HNSCC cell lines to death agonists like TNF-α and TRAIL. In this study, we have observed that birinipant also sensitizes most HPV(+) cell lines to TRAIL and TNF-α in vitro. The IC50 of birinipant was under 50nM for HPV(+) UPCI-SCC-90 and UM-SCC-47 cell lines, when combined with TNF-α or TRAIL. To explore the therapeutic potential of enhancing TRAILR mediated death signaling in HPV(+) HNSCC cells, we investigated the effects of an agonistic polyclonal TRAILR2 antibody. Treatment of ...
YC-137 is a BCL-2 inhibitor, which selectively induces apoptosis of Bcl-2-overexpressing cells and disrupts its interaction with Bid BH3, thereby blocking the anti-apoptotic activity of Bcl-2.
However the bid may have backfired, as it only really offers proof that German officials were well aware that migrants were liable to grope German girls
Bid Manager - 12 month Fixed Term Contract 03 February, 2021 will include:Coordinating and programme managing the end-to-end bid process for strategic pur...
We list competing bids of the same amount to indicate what prompted an autobid to be placed. Otherwise, it would be unclear as to why an autobid was increased.. For Example, Item 100 has a current amount of $100 and a bid increment of $50. John placed an autobid at 7:00pm with a maximum amount of $200. John is winning at $150. Jill placed a bid for $200 at 7:30pm. Johns bid is increased to $200 by our system. John wins because he committed to the amount earlier than Jill. The list shows both John and Jill at $200 so we can see what prompted Johns bid to increase.. ...
We list competing bids of the same amount to indicate what prompted an autobid to be placed. Otherwise, it would be unclear as to why an autobid was increased.. For Example, Item 100 has a current amount of $100 and a bid increment of $50. John placed an autobid at 7:00pm with a maximum amount of $200. John is winning at $150. Jill placed a bid for $200 at 7:30pm. Johns bid is increased to $200 by our system. John wins because he committed to the amount earlier than Jill. The list shows both John and Jill at $200 so we can see what prompted Johns bid to increase.. ...
To ensure that the impact on town centre businesses with regards to retail and leisure displacement is minimised, a form of supporting funding for the town centre should be put in place to compensate and there should be a focus on efforts and resources to enable the town centre to develop its own offer. The BID is very keen to support partners in the creation of a new town centre plan. ...
Speculation is mounting that US pharmaceutical giant Pfizer is set to make a hostile bid for AstraZeneca after its £63 billion takeover offer was spurned. The UK company said the offer substantially undervalued the business, forcing
Im 31 weeks and this weekend have started to notice a pattern in BH. I get them from 8-10 every morning and theyre actually pretty painful. I thought I was going to have to call the doc yesterday as they were timeable and not letting up. This is my3rd and I dont remember this with the other 2. Any other ladies experience this?
Recommended Review Article:. Chipuk JE, Green DR. 2008. How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? TRENDS IN CELL BIOLOGY 18(4): 157-164. Recommended Articles:. Aslan JE, Thomas G. 2009. Death by Committee: Organellar Trafficking and Communication in Apoptosis. TRAFFIC 10(10): 1390-1404. Chipuk JE, Green DR. 2009. PUMA cooperates with direct activator proteins to promote mitochondrial outer membrane permeabilization and apoptosis. CELL CYCLE 8(17): 2692-2696. Chipuk JE, Bouchier-Hayes L, Green DR. 2006. Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario. CELL DEATH AND DIFFERENTIATION 13(8): 1396-1402 Chipuk JE, Green DR. 2006. Dissecting p53-dependent apoptosis. CELL DEATH AND DIFFERENTIATION 13(6): 994-1002 Chipuk JE, Bouchier-Hayes L, Kuwana T, et al. 2005. PUMA couples the nuclear and cytoplasmic proapoptotic function of p53 . SCIENCE 309(5741): 1732-1735. Kuwana T, Bouchier-Hayes L, Chipuk JE, et al. 2005. BH3 ...
Read Preservation of Mitochondrial Structure and Function after Bid- or Bax-Mediated Cytochrome c Release, The Journal of Cell Biology on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
The proapoptotic BAX protein triggers apoptosis via the intrinsic pathway by inducing mitochondrial outer membrane permeabilization (MOMP). BAX largely exists in an inactive conformation in the cytoplasm, but under cellular stress BAX is activated by BH3-only proteins and translocates to the mitochondrial outer membrane to induce MOMP. Structural studies have revealed conformational changes at the N-terminal surface and C-terminal α9 helix that are required for BAX activation by BH3 proteins and MOMP induction, but suggest that additional mechanisms may stabilize BAX in the inactive cytosolic conformation. Garner, Reyna, and colleagues identified an autoinhibited dimeric BAX conformation in addition to the inactive monomer conformation. The BAX dimers did not induce membrane permeabilization, and, in contrast to BAX monomers, were resistant to BH3-mediated activation. Moreover, BAX dimers failed to translocate to the membrane upon BH3-induced stimulation. Crystallization studies indicated that ...
Important Notice: For ITBs over $50K, all prospective bidders must fax and email companys general information. This includes: the company name, address, phone number, fax number and email addresses, to the responsible Buyer before downloading the bid document.. Please note that: Addendums are NOT posted to the City website. Bidders must be identified as a current Vendor and on the official Plan Holders List in order to receive an addendum or revision to plans or specifications. Failure to contact this office with this pertinent information will cause a bid to be non-responsive and the bid may be rejected.. Full information regarding each individual bid can be accessed by clicking on the file numbers below. Some files will include additional documentation within the bid information, all additional information will be found at the bottom of the page and can be accessed by clicking on the provided link.. ...
Important Notice: For ITBs over $50K, all prospective bidders must fax and email companys general information. This includes: the company name, address, phone number, fax number and email addresses, to the responsible Buyer before downloading the bid document.. Please note that: Addendums are NOT posted to the City website. Bidders must be identified as a current Vendor and on the official Plan Holders List in order to receive an addendum or revision to plans or specifications. Failure to contact this office with this pertinent information will cause a bid to be non-responsive and the bid may be rejected.. Full information regarding each individual bid can be accessed by clicking on the file numbers below. Some files will include additional documentation within the bid information, all additional information will be found at the bottom of the page and can be accessed by clicking on the provided link.. ...
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An electronic person-to-person double auction-like system that facilitates trade in many differs sorts of item via the World Wide Web or similar such interface. A plurality of sellers can post details of items for sale, including a minimum bid amount and buy price for each. A buyer can create a bid basket comprising bids in respect of a plurality of heterogeneous items available for sale, together with bid-withdrawal rules defining circumstances in which respective bid(s) are to be withdrawn. Bids are binding unless withdrawn. The auction for any item continues until a buyer posts the buy price therefor or the seller accepts a bid posted therefor.
style=padding: 0.3em; margin-left:15px; border:1px solid #a9a9a9; text-align:center; font-size: 95%; background:#f5f5f5 width=160px align=right ,- ,Additional Information ,- ,[http://sp/sites/de/Bid/PSE_Due_Dates/Due_Dates_2021.pdf PS&E Due Date Chart] ,- ,[[media:103.1.6 Reviewers Checklist.docx,Reviewers Checklist]] ,- ,Forms ,- ,[http://epg.modot.org/forms/DE%202017%20Forms/BiddingContract/103.1_award_letter.docx Award Letter] ,- ,MoDOT Website ,- ,[http://www.modot.org/bidding/ MoDOT Bidding and Contracting Opportunities] ,} ==103.1.1 Introduction== The goal of MoDOTs bid opening and award process is to achieve competitive bids by packaging projects in a manner that makes them as attractive as possible to potential bidders. Methods of achieving this goal include, but are not limited to, establishing appropriate bid opening dates for the type of work, maintaining a stable bid opening schedule, and grouping or dividing projects to make them more appealing to bidders. ...
Bids and Proposals are to be mailed or hand delivered to the Procurement Lock Box located at the School Administration Building, 230 South Street, Hyannis, MA 02601. If sending FedEX or UPS, please do not require a signature for delivery. They may deposit in lock box located at the top of the ramp at the School Administration Building located at 230 South Street, Hyannis, MA 02601. It is the sole responsibility of the offeror to insure that the proposal arrives on time and at the designated place ...
Verizons top executive on Tuesday left open the possibility that the US telecom giant could make a bid for Yahoo if the Internet firm puts itself up for sale.
The SPCA has begun uplifting hordes of animals, birds and cats from a Northland farm after their owner lost a bid to appeal against
Browse the Foothill High Athletic Boosters fundraising auction powered by BiddingForGood and bid on items to help support this cause.
I was watching one eBay auction the other day for the Leica CS20 (which also runs WEC 7), with a starting bid of 75 USD. In the last 15 seconds there was a bid for 251 USD, followed immediately by a bid for 2650 USD (!), which was outbid at the end for 2700 USD. And it was listed as used! Im a CE addict, but even I dont need a fix that expensive ...
id:9119,bid:30504,uid:0,title:dam,username:Nikki1808,rating:5,pros:hmm,cons:alrite,description:its an alrite place ive heard..but check it out see fer yourself,date_added:1207013128,date_modified:null,is_external:1,external_site_name:zootoo,external_site_url:null,external_user_profile:null,status:1},{id:9118,bid:30504,uid:0,title:One of the best,username:J2C,rating:5,pros:Very smart,cons:none,description:a very great vet that you should take a visit to,date_added:1202579490,date_modified:null,is_external:1,external_site_name:zootoo,external_site_url:null,external_user_profile:null,status:1 ...
Tokopedia, Indonesias largest e-commerce platform, said it was investigating an attempted hack and claims that the details of millions of its users had
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... cancer cell's susceptibility to apoptosis via TNF-α signalling by the BH3 interacting domain death agonist and STAT proteins. ... Waiwut, P; Inujima, A; Inoue, H; Saiki, I; Sakurai, H (January 2012). "Bufotalin sensitizes death receptor-induced apoptosis ...
Apoptosis Apoptosome Bcl-2 Bcl-2-associated X protein (BAX) BH3 interacting domain death agonist (BID) Caspases Cytochrome c ... The PUMA protein is part of the BH3-only subgroup of Bcl-2 family proteins. This group of proteins only share sequence ... "Structure of the BH3 domains from the p53-inducible BH3-only proteins Noxa and Puma in complex with Mcl-1". J. Mol. Biol. 380 ( ... Webster KA (July 2006). "Puma joins the battery of BH3-only proteins that promote death and infarction during myocardial ...
Bcl-xL BH3 interacting domain death agonist (BID) Caspases Cytochrome c Noxa Mcl-1 Mitochondrion Microphthalmia-associated ... These pro-apoptotic proteins are in turn activated by BH3-only proteins, and are inhibited by the function of BCL-2 and its ... Hsu SY, Lin P, Hsueh AJ (September 1998). "BOD (Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing ... and induces cell death independent of a Bcl-2 homology 3 (BH3) domain at both mitochondrial and nonmitochondrial sites". The ...
USA BH3 interacting domain death agonist, a pro-apoptotic protein Binary integer decimal Brought in dead, a patient found dead ...
The pro-apoptotic BH3-interacting domain death agonist (Bid) is one such protein that once myristoylated, translocates to the ... Myristoylation allows for weak protein-protein and protein-lipid interactions and plays an essential role in membrane targeting ... These conformational switches can be utilized as a signal for cellular localization, membrane-protein, and protein-protein ... death receptor binding initiates the formation of the death-inducing signaling complex, a complex composed of numerous proteins ...
... bcl-x protein MeSH D12.644.360.075.718.968 - bh3 interacting domain death agonist protein MeSH D12.644.360.100 - ca(2+)- ... proto-oncogene proteins c-bcl-2 MeSH D12.644.360.075.718.100 - bcl-associated death protein MeSH D12.644.360.075.718.400 - bcl- ... 14-3-3 proteins MeSH D12.644.360.024.318 - proto-oncogene proteins c-crk MeSH D12.644.360.024.326 - proto-oncogene proteins c- ... ral gtp-binding proteins MeSH D12.644.360.525.462 - ran gtp-binding protein MeSH D12.644.360.525.475 - rap gtp-binding proteins ...
After the protein BH3 interacting-domain death agonist (Bid) has been myristoylated, it targets the protein to move to the ... but the site where the lipid binds to the protein depends both on the lipid group and protein. Prenylated proteins are proteins ... This allows for the interaction of proteins with cellular membranes and protein domains. In a dynamic role, lipidation can ... Lipid-anchored proteins (also known as lipid-linked proteins) are proteins located on the surface of the cell membrane that are ...
Apoptosis Apoptosome Bcl-2 BH3 interacting domain death agonist (BID) Caspases Cytochrome c Noxa Mitochondrion p53 upregulated ... binds the BH3 domain of other BAX or BCL-2 proteins in its active form. In the protein's inactive form, the groove binds its ... This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with ... domains (named BH1, BH2, BH3 and BH4), and can form hetero- or homodimers. These domains are composed of nine α-helices, with a ...
Apoptosis Apoptosome Bcl-2 Bcl-2-associated X protein (BAX) BH3 interacting domain death agonist (BID) Caspases Cytochrome c ... Kim JY, Ahn HJ, Ryu JH, Suk K, Park JH (2004). "BH3-only protein Noxa is a mediator of hypoxic cell death induced by hypoxia- ... Phorbol-12-myristate-13-acetate-induced protein 1 is a protein that in humans is encoded by the PMAIP1 gene, and is also known ... until displaced by BH3-only proteins". Genes Dev. 19 (11): 1294-305. doi:10.1101/gad.1304105. PMC 1142553. PMID 15901672. Oda E ...
The BH3 interacting-domain death agonist, or BID, gene is a pro-apoptotic member of the Bcl-2 protein family. Bcl-2 family ... The BH3 interacting-domain death agonist has been shown to interact with: ATR/ATRIP, BCL2, CASP2, CASP8, MCL1, and RPA. Several ... Wang K, Yin XM, Chao DT, Milliman CL, Korsmeyer SJ (1996). "BID: a novel BH3 domain-only death agonist". Genes Dev. 10 (22): ... BID is a pro-apoptotic Bcl-2 protein containing only the BH3 domain. In response to apoptotic signaling, BID interacts with ...
... as a pro-apoptotic protein due to the conserved BH3 interacting domain death agonist located at the C-terminus of the protein ... with the most extensive conservation being found at the C-terminus of the protein. The BH3 interacting-domain death agonist ( ... The C6orf222 protein contains one mammalian conserved domain: DUF3293. The protein is also predicted to contain a BH3 domain, ... A predicted BH3 domain in the C6orf222 protein was found to interact with both Bcl-2 and Bcl-xL, implicating C6orf222 as being ...
... has been shown to interact with: BH3 interacting domain death agonist, CRADD, and Caspase 8. The Proteolysis Map ... a long pro-domain that is similar to that of caspase 9 and contains a protein interaction domain known as a CARD domain. Pro- ... Together with RAIDD and p53-induced protein with a death domain ([PIDD])(LRDD), caspase 2 has been shown to form the so-called ... including RIP-associated Ich-1/Ced-3-homologue protein with a death domain (RAIDD), apoptosis repressor with caspase ...
BH3 interacting-domain death agonist. *BRAF (gene). *Bone morphogenetic protein 10. *C-Met ... Public domainPublic domainfalsefalse This image is in the public domain because it contains materials that originally came from ... Email the source site if it is not clearly stated that this specific work is in the public domain. ... the NIH frequently uses commercial images which are not public domain. ...
... bcl-x protein MeSH D12.776.476.075.718.937 - bh3 interacting domain death agonist protein MeSH D12.776.476.150.300.100 - casein ... bcl-associated death protein MeSH D12.776.476.075.718.400 - bcl-2-associated x protein MeSH D12.776.476.075.718.425 - bcl-2 ... smad1 protein MeSH D12.776.476.024.417.500.200 - smad2 protein MeSH D12.776.476.024.417.500.300 - smad3 protein MeSH D12.776. ... smad proteins, inhibitory MeSH D12.776.476.024.417.249.600 - smad6 protein MeSH D12.776.476.024.417.249.700 - smad7 protein ...
BH3 interacting-domain death agonist) Luis Moroder, G. Andrew Woolley, Rudolf K. Allemann, Jean Chmielewski N. Umezawa; Y. Noro ... "Reversible Photocontrol of DNA Binding by a Designed GCN4-bZIP Protein". Biochemistry. 45 (19): 6075-6084. CiteSeerX 10.1.1.555 ... 2007). "Investigation into the P3 binding domain of m-calpain using photoswitchable diazo- and triazene-dipeptide aldehydes: ... "Light triggers cancer death switch". Molecular BioSystems. 9 (11): 2597-603. doi:10.1039/C3MB70246D. PMID 23942570. Retrieved ...
This protein shares a critical BH3 domain with other death-promoting proteins, BAX and BAK. Bcl-2-interacting killer has been ... a BH3-containing mouse protein that interacts with Bcl-2 and Bcl-xL, is a potent death agonist". J. Biol. Chem. 273 (14): 7783- ... a novel death-inducing protein shares a distinct sequence motif with Bcl-2 family proteins and interacts with viral and ... Han J, Sabbatini P, White E (1996). "Induction of apoptosis by human Nbk/Bik, a BH3-containing protein that interacts with E1B ...
The protein encoded by this gene contains a Bcl-2 homology domain 3 (BH3). It has been shown to interact with other members of ... 1996). "BID: a novel BH3 domain-only death agonist". Genes Dev. 10 (22): 2859-69. doi:10.1101/gad.10.22.2859. PMID 8918887. Zha ... Hsu SY, Lin P, Hsueh AJ (November 1998). "BOD (Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing ... 2002). "Identification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosis". Mol. ...
1998). "Blk, a BH3-containing mouse protein that interacts with Bcl-2 and Bcl-xL, is a potent death agonist". J. Biol. Chem. ... a conserved nuclear phosphoprotein that contains multiple tetratricopeptide repeats and binds specifically to SH2 domains". J. ... The tyrosine-protein kinase BLK has been shown to interact with UBE3A. ENSG00000285369 GRCh38: Ensembl release 89: ... 1993). "Mapping of sites on the Src family protein tyrosine kinases p55blk, p59fyn, and p56lyn which interact with the effector ...
Identification of a BH-3 domain and analysis of its binding to mutant BCL-2 and BCL-XL proteins". J. Biol. Chem. 272 (49): ... The BCL2 associated agonist of cell death (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family which is involved in ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". EMBO ... "The proapoptotic BH3-only protein BAD transduces cell death signals independently of its interaction with Bcl-2". Cell Death ...
Milliman CL, Korsmeyer SJ, Wang K, Yin XM, Chao DT (1996). "BID: a novel BH3 domain-only death agonist". Genes Dev. 10 (22): ... The BH3-only subset of the Bcl-2 family of proteins contain only a single BH3-domain. The BH3-only members play a key role in ... Arbel, Nir; Shoshan-Barmatz, Varda (2010-02-26). "Voltage-dependent anion channel 1-based peptides interact with Bcl-2 to ... or those proteins that have only the BH3 domain (e.g. Bim Bid and BAD) All proteins belonging to the Bcl-2 family contain ...
Autophagy Autoschizis Bcl-2 BH3 interacting domain death agonist (BID) Calpains Caspases Cell damage Cornification Cytochrome c ... Research on the corn poppy (Papaver rhoeas) has revealed that proteins in the pistil on which the pollen lands, interact with ... Programmed cell death (or PCD) is the death of a cell in any form, mediated by an intracellular program. PCD is carried out in ... Some categorize death in those organisms as unregulated apoptosis-like cell death. Biologists had long suspected that ...
Pierrat B, Ito M, Hinz W, Simonen M, Erdmann D, Chiesi M, Heim J (May 2000). "Uncoupling proteins 2 and 3 interact with members ... Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ (1997). "Serine phosphorylation of death agonist BAD in response to survival ... "Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function". Mol. ... This article incorporates text from the United States National Library of Medicine, which is in the public domain.. ...
... and Fas-associated death domain protein (FADD). cIAP1/2 can inhibit TNF-α signaling by binding to TRAF2. FLIP inhibits the ... Bax or Bak are activated by the activation of BH3-only proteins, part of the Bcl-2 family. ... Akt phosphorylates and inhibits Bas (a Bcl-2 family member), causing Bas to interact with the 14-3-3 scaffold, resulting in Bcl ... therefore overexpression leads to a decrease in the amount of proapoptotic agonists. As a consequence, the balance of anti- ...
... and Fas-associated death domain protein (FADD). cIAP1/2 can inhibit TNF-α signaling by binding to TRAF2. FLIP inhibits the ... Bax or Bak are activated by the activation of BH3-only proteins, part of the Bcl-2 family[citation needed]. ... Akt phosphorylates and inhibits Bad (a Bcl-2 family member), causing Bad to interact with the 14-3-3 scaffold, resulting in Bcl ... therefore overexpression leads to a decrease in the amount of proapoptotic agonists. As a consequence, the balance of anti- ...
NATURAL PROTEINS \ pro-643 for more molecular products just contact us ... Recombinant Mouse BH3 Interacting Domain Death Agonist GST RECOMBINANT & ... NATURAL PROTEINS mus musculus murine Recombinant Mouse BH3 Interacting Domain Death Agonist GST RECOMBINANT & NATURAL PROTEINS ... NATURAL PROTEINS. Related products : Recombinant Mouse BH3 Interacting Domain Death Agonist GST RECOMBINANT & NATURAL PROTEINS ...
Protein Coding), BH3 Interacting Domain Death Agonist, including: function, proteins, disorders, pathways, orthologs, and ... BH3-interacting domain death agonist) ELISA, Immunotag™ Human Cleaved BID/TBID (Cleaved BH3-interacting domain death agonist) ... Protein Symbol:. P55957-BID_HUMAN. Recommended name:. BH3-interacting domain death agonist. Protein Accession:. P55957. ... Protein Products. * G Biosciences Human BID/BH3-interacting domain death agonist, Liquid ...
BH3-interacting domain death agonist; cFLIP, cellular FLICE-inhibitory protein; CUL3, cullin 3; DISC, death-inducing signaling ... Wiezorek J, Holland P, Graves J. Death receptor agonists as a targeted therapy for cancer. Clin Cancer Res. 2010;16(6):1701- ... Opposing unfolded-protein-response signals converge on death receptor 5 to control apoptosis. Science. 2014;345(6192):98-101. ... Triggering cell death: The crystal structure of Apo2L/TRAIL in a complex with death receptor 5. Mol Cell. 1999;4(4):563-571. ...
... we show that peptides corresponding to the BH3 domains of Bcl-2 family BH3-only proteins have dual functions. Several BH3 ... peptides relieved the inhibition of Bax caused by the antiapoptotic Bcl-x(L) and/or Mcl-1 proteins, some displaying a spe … ... BH3 Interacting Domain Death Agonist Protein * Bcl-2-Like Protein 11 * Carrier Proteins / metabolism ... we show that peptides corresponding to the BH3 domains of Bcl-2 family "BH3-only" proteins have dual functions. Several BH3 ...
The use of BH3 mimetics, mimicking pro-apoptotic activator or sensitizer proteins of the intrinsic apoptotic pathway, is ... and specific BH3 mimetics as sensitizers for cell death and gives an outlook how they could be effectively used for the therapy ... The use of BH3 mimetics, mimicking pro-apoptotic activator or sensitizer proteins of the intrinsic apoptotic pathway, is ... and specific BH3 mimetics as sensitizers for cell death and gives an outlook how they could be effectively used for the therapy ...
Apoptosis Regulatory Proteins / physiology* * BH3 Interacting Domain Death Agonist Protein / metabolism* * Bcl-2-Like Protein ... BH3 profiling identifies cells that require BCL-2 for survival and predicts sensitivity to the BCL-2 antagonist ABT-737. BCL-2 ... BH3 profiling identifies three distinct classes of apoptotic blocks to predict response to ABT-737 and conventional ... Using a panel of 18 lymphoma cell lines, we show that a strategy we have developed, BH3 profiling, can identify apoptotic ...
... instead displaying upregulation of the proapoptotic protein BH3-interacting domain death agonist (4.3 fold). Adolescent protein ... A further 12 proteins were significantly altered in both adolescents and adults. In adults, protein changes were generally ... A further 12 proteins were significantly altered in both adolescents and adults. In adults, protein changes were generally ... Results indicated age-specific changes in protein expression, with paroxetine significantly altering expression of 8 proteins ...
The mitochondrial carrier homologue-2 (MTCH2). Binds the BH3-interacting domain death agonist, BID. Regulated (induced) by the ... It has been proposed that its transport function has been lost (Robinson et al., 2012). Surprisingly, this protein has been ...
BH3 interacting domain death agonist 581 BAX; BCL2 associated X, apoptosis regulator 4217 MAP3K5; mitogen-activated protein ... BH3 interacting domain death agonist K02159 BAX; apoptosis regulator BAX K04426 MAP3K5; mitogen-activated protein kinase kinase ... 2776 GNAQ; G protein subunit alpha q 5578 PRKCA; protein kinase C alpha 5579 PRKCB; protein kinase C beta 5582 PRKCG; protein ... 2770 GNAI1; G protein subunit alpha i1 2773 GNAI3; G protein subunit alpha i3 2771 GNAI2; G protein subunit alpha i2 23236 ...
... receptor-interacting serine/threonine-protein kinase 1; BID, BH3 interacting-domain death agonist; BAX, Bcl-2-associated X ... Fas-associated protein with death domain; CASP, caspase; RIP1, ... RIP1 protein-dependent assembly of a cytosolic cell death ... Similar to IGF1R, FGFR4 is a transcriptional target of the PAX3-FOXO1 fusion protein leading to increased protein expression ( ... In this regard, targeting of RTKs, downstream proteins, Hedgehog signaling, DDR, cell-cycle proteins and the epigenome shows ...
BH3 interacting domain death agonist (BID); BCL2 antagonist killer 1 (BAK1); tumor necrosis factor (ligand) superfamily, member ... transmembrane protein 74 (TMEM74); death-associated protein kinase 1 (DAPK1); eukaryotic translation initiation factor 4 gamma ... Figure 2: (a) Effects of IL-1β (1 ng/mL) or F. nucleatum (OD: 0.025) on CTSS protein level in supernatants at 1 d and 2 d, as ... The changes in CTSS gene expression by IL-1β and F. nucleatum were further studied at protein level. As analyzed by ELISA, F. ...
0 (BH3 Interacting Domain Death Agonist Protein); 0 (Bad protein, mouse); 0 (Bak1 protein, mouse); 0 (Bax protein, mouse); 0 ( ... 0 (BCL9L protein, human); 0 (BH3 Interacting Domain Death Agonist Protein); 0 (BID protein, human); 0 (DNA-Binding Proteins); 0 ... BH3 Interacting Domain Death Agonist Protein); 0 (BID protein, human); 0 (GABRB1 protein, human); 0 (NOS1AP protein, human); 0 ... 0 (BH3 Interacting Domain Death Agonist Protein); 0 (BID protein, human); 0 (MIRN20 microRNA, human); 0 (MicroRNAs); 0 (TNF- ...
... which incorporates a GST tag to the N-terminal of each protein. The proteins were expressed by transfection of the cloned ... BH3 interacting domain death agonist (BID), transcript variant 2, mRNA. NM_001196.3. NP_001187.1. 972. ... Sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3B, mRNA (cDNA clone MGC:18122 IMAGE: ... BCL2-associated agonist of cell death (BAD), transcript variant 1, mRNA. NM_004322.3. NP_004313.1. 22. ...
BH3-interacting domain death agonist. Protein. P55957 (Uniprot-TrEMBL) Biglycan. Protein. P21810 (Uniprot-TrEMBL) CCL2. ... KE1: Cell injury/death (KE55). Histone H2AX. Cytochrome C. AIF1. BH3-interacting domain death agonist. BAX. Calpain-1 catalytic ... Protein. E9PRM1 (Uniprot-TrEMBL) Caspase-3. Protein. A8MVM1 (Uniprot-TrEMBL) Caspase-9. Protein. F8VWA5 (Uniprot-TrEMBL) ... Protein alkylation. Collagen accumulation. KER 269. MIE: Protein alkylation (KE244). Stressors. Proto-oncogene c-Rel. Toll-like ...
Home > Protein > BID human. mouse. rat. New Protein Search:. BH3-interacting domain death agonist ... Protein Mutation Frequency in Cancer. The lollipop plot above illustrates recurrent (observed in 3 or more out of 4440 TCGA ...
BH3 interacting domain death agonist. BMDM. bone marrow-derived macrophages. BMEC. bovine mammary epithelial cells ... MIR-interacting saposin-like protein or canopy 2 homolog or transmembrane protein 4 ... coiled-coil, moesin-like BCL2 interacting protein or autophagy related 6 homolog ... lectin, galactoside-binding, soluble, 3 or IgE-binding protein or laminin-binding protein ...
BID, BH3 interacting-domain death agonist.. Prior studies have shown that activation of CD95 can stimulate the induction of LC3 ... or the linker protein Fas-associated death domain protein expression suppressed the toxicity enhancing activity of sildenafil ( ... Knock down of CD95 or Fas-associated death domain protein suppressed drug combination toxicity. Combination toxicity was also ... or siRNA molecules to knock down expression of CD95 or Fas-associated death domain protein (FADD) (siCD95, siFADD). Thirty-six ...
BH3 interacting domain death agonist GraphId=dde, ,Graphics Color=000000 CenterX=8790.0 CenterY=4400.0 Width=900.0 ... harakiri BCL2 interacting protein (conta... GraphId=c3d, ,Graphics Color=000000 CenterX=9230.0 CenterY=5010.0 Width= ... TNFRSF1A-associated via death domain GraphId=e0c GroupRef=d59c4, ,Graphics Color=000000 CenterX=1400.0 CenterY=3320.0 ... TNFRSF1A-associated via death domain GraphId=d39 GroupRef=f44cf, ,Graphics Color=000000 CenterX=7610.0 CenterY=3040.0 ...
BH3 Interacting Domain Death Agonist ProteinIBA 01/2010. 1. Cytochromes c (Cytochrome c)IBA 01/2010. ...
Bcl-2-like protein 4; Bid, BH3-interacting-domain death agonist; tBid, truncated Bid; APAF-1, apoptotic protease activating ... Fas-associated protein with death domain; TRADD, tumor necrosis factor receptor type 1-associated death domain protein; RIG-I, ... Although caspase 8 is able to bind FADD (Fas-associated adaptor protein with death domain) in the absence of Sam68, the complex ... Nuclear protein Sam68 interacts with the enterovirus 71 internal ribosome entry site and positively regulates viral protein ...
BH3 domain-only protein, BH3 interacting domain death agonist * 645001 Size 25 µg ... Phospho-Proteins (11) Postsynaptic proteins (25) Proteases (18) Protein Kinases/Phosphatase (42) Protein Modifiers (4) Siglec ... Protein Misfolding and Aggregation (418) Protein Synthesis (66) Protein Trafficking and Clearance (253) Signal Transduction ( ... Protein Lin-28 Homolog A,Lin-28A, CSDD1,ZCCHC1, Zinc Finger CCHC Domain-Containing Protein 1 ...
... p53-induced death domain-containing protein 1 isoform X1 112922873 CASP8; caspase-8 112917438 BID; BH3-interacting domain death ... BH3 interacting domain death agonist K02159 BAX; apoptosis regulator BAX K10131 PMAIP1; phorbol-12-myristate-13-acetate-induced ... F-box and WD-40 domain protein 2 K10262 FBXW4; F-box and WD-40 domain protein 4 K10263 FBXW5; F-box and WD-40 domain protein 5 ... F-box and WD-40 domain protein 7 K10264 FBXW8; F-box and WD-40 domain protein 8 K10265 FBXW9; F-box and WD-40 domain protein 9 ...
... of the BH3 interacting domain death agonist ( BID) gene as a risk factor in Korean patients with ossification of... ... Wang H, Yang ZH, Liu DM et al (2008) Association between two polymorphisms of the bone morpho-genetic protein-2 gene with ... Association between BH3 interacting domain death agonist (BID) gene polymorphism and ossification of the posterior longitudinal ... The purpose of this study was to investigate single nucleotide polymorphisms (SNPs) of the BH3 interacting domain death agonist ...
b, antibody HPR000722 raised against the 22-kDa BH3-interacting domain death agonist (BID) transcribed from chromosome 22. c, ... Protein Atlas for Cancer Tissues-. The protein atlas also contains a summary page for the protein profiles found in the 20 ... Altogether more than 700 proteins were analyzed representing all major types of protein families, i.e. protein receptors, ... The protein may play a role in central nervous system development by interacting with growth factors implicated in motor neuron ...
The mitochondrial carrier homologue-2 (MTCH2). Binds the BH3-interacting domain death agonist, BID. Regulated (induced) by the ... Domain. Kingdom/Phylum. Protein(s). *2.A.29.1.1. Mitochondrial ATP/ADP antiporter (SLC25A5) facilitates exchange of ADP and ATP ... has a 500 residue N-terminal hydrophilic domain as well as a C-terminal 100 residue hydrophilic domain. Both domains are ... The mitochondrial presenilin-associated protein (PSAP; MTCH1) binds to the PDZ domain (a QFYI motif) C-terminus of presenilin. ...
The BH3 interacting-domain death agonist, or BID, gene is a pro-apoptotic member of the Bcl-2 protein family. Bcl-2 family ... BH3 interacting-domain death agonist. The BH3 interacting-domain death agonist, or BID, gene is a pro-apoptotic member of the ... BID is a pro-apoptotic Bcl-2 protein containing only the BH3 domain. In response to apoptotic signaling, BID interacts with ... BID is a pro-apoptotic Bcl-2 protein containing only the BH3 domain. In response to apoptotic signaling, BID interacts with ...
The BH3 interacting-domain death agonist, or BID, gene is a pro-apoptotic member of the Bcl-2 protein family. Bcl-2 family ... BID is a pro-apoptotic Bcl-2 protein containing only the BH3 domain. In response to apoptotic signaling, BID interacts with ... This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/BH3_interacting-domain_death_agonist ... domains (named BH1, BH2, BH3 and BH4), and can form hetero- or homodimers. Bcl-2 proteins act as anti- or pro-apoptotic ...
... such as B-cell lymphoma 2 protein family members (pro- and antiapoptotic), inhibitor of apoptosis proteins, and the foremost ... Owing to the fact that apoptosis causes minimal inflammation and damage to the tissue, apoptotic cell death-based therapy has ... and therapeutic strategies adopted to target these specific proteins/pathways that have entered clinical trials. ... cellular FLICE inhibiting proteins. BID:. BH3 interacting-domain death agonist protein. BAD:. Bcl-2-associated death promoter ...
Viral Proteins/*metabolism; Hepacivirus/*metabolism; Adult; Middle Aged; Aged; BH3 Interacting Domain Death Agonist Protein/ ... We previously showed that HCV proteins down-regulate expression of BH3-only Bcl2 interacting domain (Bid) in hepatocytes of HCV ... We show that the nonstructural HCV viral protein NS5A is sufficient to activate a calpain cysteine protease, leading to ... Calpain activation by hepatitis C virus proteins inhibits the extrinsic apoptotic signaling pathway. Simonin, Y.; Disson, O.; ...
ELISA Kit DIY Materials for BH3 Interacting Domain Death Agonist (Bid). Product No.: KSA629Hu01. Organism species: Homo sapiens ... ELISA Kit DIY Materials for S100 Calcium Binding Protein A8 (S100A8). Product No.: KSB792Mu01. Organism species: Mus musculus ( ... ELISA Kit DIY Materials for BH3 Interacting Domain Death Agonist (Bid). Product No.: KSA629Ra01. Organism species: Rattus ... ELISA Kit DIY Materials for C Reactive Protein (CRP). Product No.: KSA821Ra01. Organism species: Rattus norvegicus (Rat). ...
  • This gene encodes a death agonist that heterodimerizes with either agonist BAX or antagonist BCL2, and thus regulate apoptosis. (genecards.org)
  • We previously showed that HCV proteins down-regulate expression of BH3-only Bcl2 interacting domain (Bid) in hepatocytes of HCV transgenic mice. (cnrs.fr)
  • This gene encodes a death agonist that heterodimerizes with either agonist BAX or antagonist BCL2. (genetex.com)
  • This prevents BCL2-associated agonist of cell death ( BAD ) phosphorylation and leads to apoptosis in COS-7 cells. (bio-rad.com)
  • FLIP (FLICE-inhibitory protein), anti-apoptotic members of the Bcl2 family and inhibitors of apoptosis (IAP) are the main three groups of anti-apoptotic genes that counteract caspase activation through both the extrinsic and intrinsic apoptotic pathways.Modulation of the apoptotic machinery during viral and bacterial infections, as well as in various malignancies, is a wellestablished mechanism that promotes the survival of affected cells. (nih.gov)
  • HPFs exposed to TEGDMA showed statistically significant increases in multiple pro-apoptotic proteins such as BH3-interacting domain death agonist (BID), BCL2 interacting protein (BIM), caspase 3, caspase 8, TNF-related apoptosis-inducing ligand receptor 1 (TRAILR 1), TRAILR 2, Bcl-2-associated X protein (BAX), and cytochrome c at 24 hours. (umich.edu)
  • The antiapoptotic protein BCL2 is a promising potential target in the treatment of CTCL. (bloodjournal.org)
  • In healthy cells, anoikis is mostly governed by B-cell lymphoma-2 (BCL2) protein family members. (biologists.org)
  • In this Review, we discuss how a pro-apoptotic subgroup of the BCL2 protein family, known as the BH3-only proteins, controls apoptosis and anoikis during mammary gland homeostasis and to what extent their inhibition confers tumor suppressive functions in metastatic breast cancer. (biologists.org)
  • Specifically, the role of the two pro-apoptotic BH3-only proteins BCL2-modifying factor (BMF) and BCL2-interacting mediator of cell death (BIM) will be discussed here. (biologists.org)
  • A simple bioinformatics strategy identified a candidate granzyme B cleavage site in the widely expressed BNIP-2 (BCL2/adenovirus E1B-19K protein-interacting protein 2). (portlandpress.com)
  • Both mechanisms interrupt the binding between B-cell lymphoma 2 (BCL2) and BCL2 associated X protein (BAX), which leads to the oligomerization of BAX and eventually permeabilization of the mitochondrial membrane [17]. (termedia.pl)
  • Bcl-XL is a major anti-apoptotic protein in the Bcl2 family whose overexpression is more widely observed in human lung cancer cells than that of Bcl2, suggesting that Bcl-XL is more biologically relevant and therefore a better therapeutic target for lung cancer. (ufl.edu)
  • Fluorescence polarization assay reveals that BXI-61 and BXI-72 preferentially bind to Bcl-XL protein but not Bcl2 in vitro with high binding affinities. (ufl.edu)
  • Two important questions on the molecular mechanism of the B cell CLL/lymphoma 2 (BCL2) proteins involve the interaction network between pro- and antiapoptotic members and the role of their translocation to the mitochondrial membrane during apoptosis. (semanticscholar.org)
  • Peptide mass fingerprinting identified this protein as Bid, a BH3 domain- containing protein known to interact with both Bcl2 and Bax. (elsevier.com)
  • CASP8 cleaves this encoded protein, and the COOH-terminal part translocates to mitochondria where it tr. (genecards.org)
  • Besides having this derepression function, the Bid and Bim peptides activated Bax directly and were the only BH3 peptides tested that could potently induce cytochrome c release from mitochondria in cultured cells. (nih.gov)
  • The intrinsic apoptotic pathway engages caspases via members of the BCL-2 protein family and the mitochondria in reaction to severe cellular damage or stress. (jci.org)
  • We describe here a novel pathway of endolysosomal processing of mitochondria, activated in response to canonical BH3-only proteins and mitochondrial depolarization. (elsevier.com)
  • Subsequently, in an E3 ligase-dependent manner, XIAP rapidly localizes inside all the mitochondria, and XIAP-mediated mitochondrial ubiquitylation catalyses interactions of Rab membrane targeting components Rabex-5 and Rep-1 (RFP-tagged Rab escort protein-1), and Rab5- and Rab7-positive endolysosomes, at and within mitochondrial membrane compartments. (elsevier.com)
  • Furthermore, XZ-1 up-regulated the proapoptotic proteins including cleaved caspases (cysteine-dependent aspartate-specific protease) (-3, -8, and -9), Fas, Bax, and Bid, and facilitated the release of cytochrome c from mitochondria to the cytoplasm. (bioscirep.org)
  • The two pathways are also connected by the ability of active caspase 8 to activate Bid (BH3-interacting domain death agonist) - tBid (truncated Bid) is a proapoptotic molecule that can induce release of cytochrome c from the mitochondria and thus initiate the intrinsic pathway. (nih.gov)
  • Purified mitochondria from Bid knockout mice, but not from Bax knockout mice, failed to release cytochrome c in response to autologous S-100 and GrB.Also, Bak-deficient mitochondria did not release cytochrome c in response to GrB-treated cytosol unless recombinant Bak protein was added.These results are the first to report a role for Bak in GrB-mediated mitochondrial apoptosis. (nih.gov)
  • Also, Bak-deficient mitochondria did not release cytochrome c in response to GrB-treated cytosol unless recombinant Bak protein was added. (nih.gov)
  • BH3 proteins have been shown to localize to mitochondria after apoptotic stimuli, where they bind to Bcl-2 family members and induce mitochondrial events associated with apoptosis, including the release of cytochrome c into the cytosol ( 4 ). (pnas.org)
  • The activity of these proteins is related to the release of apoptogenic factors, sequestered in the mitochondria, to the cytoplasm, probably through the formation of ion and/or protein transport channels. (jove.com)
  • Caspase-2 failed to induce cytochrome c release from mitochondria with Bid -/- background, and the release could be restored by addition of the wild-type Bid protein, but not by Bid with the caspase-2 cleavage site mutated. (elsevier.com)
  • In response to pro-apoptotic signals (from pro-apoptotic proteins such as Bax), cytochrome c is released into the cell by the mitochondria, and they bind to a protein known as Apaf-1. (scientificamerican.com)
  • Various apoptotic stimuli induce expression and/or activation of specific BH3-only family members, which translocate to the mitochondria and initiate Bax/Bak-dependent apoptosis. (genenames.org)
  • p15 BID translocates to mitochondria as an integral membrane protein. (bosterbio.com)
  • A loss of the MMP by any mechanism leads to functional and structural collapse of the mitochondria and cell death. (oatext.com)
  • The severe acute respiratory syndrome coronavirus (SARS-CoV) escapes the innate immune response by translocating its ORF-9b to mitochondria and promotes proteosomal degradation of dynamin-like protein (Drp1) leading to mitochondrial fission. (oatext.com)
  • Through direct interaction with the voltage-dependent anion channel (VDAC), proapoptotic members of the Bcl-2 family such as Bax and Bak induce apoptogenic cytochrome c release in isolated mitochondria, whereas BH3-only proteins such as Bid and Bik do not directly target the VDAC to induce cytochrome c release. (nih.gov)
  • tBID is the active from of the protein and it redistributes from the CYTOSOL to MITOCHONDRIA to promote release of CYTOCHROME C. (bvsalud.org)
  • We report here the purification of a cytosolic protein that induces cytochrome c release from mitochondria in response to caspase-8, the apical caspase activated by cell surface death receptors such as Fas and TNF. (elsevier.com)
  • In addition, Ky2 released cytochrome c from mitochondria to cytosol through the regulation of mitochondria-related proteins (Bid, Bim, and Bcl-xL). (elsevier.com)
  • The caspase-10 was dispensable for enhancement of cisplatin/LA-12 and TRAIL combination-induced cell death and stimulation of Bid cleavage. (bireme.br)
  • Association of adaptor molecules (FADD - Fas-associated death domain protein, TRADD-TNF receptor associated death domain protein) induces the formation of DISC (death inducing signaling complex), which activates caspase 8 and subsequently caspase 3. (nih.gov)
  • Cytochrome c associates with Apaf-1 and procaspase 9 to form the apoptosome, a multimeric protein complex that induces cleavage of inactive caspase 9 to its active form. (nih.gov)
  • Several reports have demonstrated that caspase-8, and its substrate BID, are frequently activated in response to certain apoptotic stimuli in a death receptor-independent manner. (wikipedia.org)
  • Depending on individual (patho-) physiological circumstances, cell-type and involved receptor-ligand system, cellular responses range from activation of pro-inflammatory and potentially pro-tumoural pathways such as nuclear factor κB (NFκB), to caspase-dependent and -independent mechanisms of cell death induction. (mdpi.com)
  • Early in the process, leelamine-mediated killing was a caspase-independent event triggered by cholesterol accumulation, as depletion of cholesterol using β-cyclodextrin treatment attenuated the cell death and restored the subcellular structures identified by electron microscopy. (aacrjournals.org)
  • Granzyme B triggers apoptosis via the cleavage of a repertoire of cellular proteins, leading to caspase activation and mitochondrial depolarization. (portlandpress.com)
  • Minocycline directly targets the mitochondrial proteins and impedes the release of factors responsible for cell death which could either be caspase-dependent (Smac/Diablo, cytochrome c (cyt c)) or caspase independent (apoptosis-inducing factor) [6]. (termedia.pl)
  • HIF-1α stabilizes the p53 pathway, whereas FAS mediates cell death by activation of caspase 8 and increase of BH3 interacting domain death agonist (BID). (termedia.pl)
  • Changes in Bax (proapoptotic Bcl-2-associated X protein), cytochrome c , and caspase-9 cleavage in the cytosolic and mitochondrial fractions of neural retinal tissues were measured by Western blot analysis. (arvojournals.org)
  • The results demonstrated that the protein expression levels of Bcl‑2 were decreased, whereas those of Bax, cleaved poly ADP‑ribose polymerase, cleaved caspase‑9 and p53 were upregulated in a dose‑dependent manner in apigenin‑treated cells compared with those noted in untreated cells. (spandidos-publications.com)
  • Most applications of peptides in apoptosis research are so far related to caspases, caspase regulatory proteins, such as LAPs and Smac, and proteins of the Bcl-2 family. (jove.com)
  • Ciglitazone kills cervical cancer cells by activating death receptor signalling pathway, caspase cascade and BH3 interacting-domain death agonist (Bid) cleavage through the up-regulation of Death Receptor 4 (DR4)/DR5 and soluble and membrane-bound TNF related apoptosis inducing ligand (TRAIL). (oncotarget.com)
  • Citric acid increased the level of Bcl-2-associated X protein (BAX) and reduced the levels of B-cell lymphoma-2 (BCL-2), B-cell lymphoma-extra large (BCL-XL) and activated caspase-9 and caspase-3, which subsequently induced apoptosis via caspase-dependent and caspase-independent pathways. (iiarjournals.org)
  • Citric acid also activated death receptors and increased the levels of caspase-8, activated BH3 interacting-domain death agonist (BID) protein, Apoptosis-inducing factor (AIF), and Endonuclease G (EndoG). (iiarjournals.org)
  • Apoptotic cell death can be initiated by either an intrinsic or extrinsic pathway, both of which converge at the activation of caspase-3. (psu.edu)
  • Cell death pathways are opposed by anti-apoptotic proteins that protect mitochondrial membrane integrity (Bcl-x, Bcl-2), block caspase activity (IAPs) or prevent signaling via death receptors (the adaptor protein, FLIP). (psu.edu)
  • Oligomerization of these receptors allow the recruitment of the adaptor protein Fas-associated death domain (FADD), which subsequently stimulates the formation of death-inducing signaling complex (DISC) through recruitment of the pro-caspase-8 ( 3 , 4 ). (spandidos-publications.com)
  • Activation of pro-caspase-8 within the DISC, by proximity, activates either a cascade of caspase-cleavage leading to activation of caspase-3, −6, and −7 (extrinsic pathway) or stimulates the mitochondrial pathway (intrinsic pathway) via cleavage of the BH3-interacting domain death agonist (Bid) to truncated Bid (tBid)/caspase-3, inducing an irreversible cell death ( 5 ). (spandidos-publications.com)
  • In addition, due to the fact that multiple caspases cleave Bid at the same site in vitro, the identity of the Bid-cleaving caspase during death receptor signaling remains uncertain. (elsevier.com)
  • In contrast, the caspase-resistant mutant Bid D60E and a BH3 defective mutant Bid G94E failed to restore TRAIL-induced apoptosis. (elsevier.com)
  • Together, these results for the first time establish that cleavage by caspase 8 and the subsequent association with the outer mitochondrial membrane are two critical events that activate Bid during death receptor-mediated apoptosis. (elsevier.com)
  • It is a pro-apoptotic protein that is activated by caspase cleavage. (bvsalud.org)
  • A C-terminal fragment of Bid protein that is produced by caspase cleavage. (bvsalud.org)
  • We show that in SW620 cells, although caspase-8 is recruited and activated at the death-inducing-signalling complex and Bid is cleaved, this does not lead to caspase-9 activation. (edu.au)
  • Activation of caspase 8 followed by cleavage of the proapoptotic protein Bid only occurs in non-neural cells. (elsevier.com)
  • Gene Ontology (GO) annotations related to this gene include ubiquitin protein ligase binding and death receptor binding . (genecards.org)
  • In contrast, clinical attempts to stimulate the extrinsic pathway with proapoptotic receptor agonists (PARAs) have been disappointing, despite compelling preclinical efficacy with this class of agents. (jci.org)
  • We concentrated on the most common classes of targeted therapies investigated in rhabdomyosarcoma to date, including those directed against receptor tyrosine kinases and associated downstream signaling pathways, the Hedgehog signaling pathway, apoptosis pathway, DNA damage response, cell-cycle regulators, oncogenic fusion proteins, and epigenetic modifiers. (aacrjournals.org)
  • Combination toxicity was also abolished by necrostatin or receptor interacting protein 1 knock down. (aspetjournals.org)
  • receptor (TNFRSF)-interacting serine-th. (wikipathways.org)
  • Moreover, pharmacological inhibitors of calpains restore both the physiological levels of Bid and the sensitivity of cells toward a death receptor-mediated apoptotic signal. (cnrs.fr)
  • Bufotalin sensitizes death receptor-induced apoptosis via Bid- and STAT1-dependent pathways" (PDF). (wikipedia.org)
  • We report that expression of canonical BH3-only proteins, tBid, BimEL, Bik, Bad, and mitophagy receptor mutants of atypical BH3-only proteins, Bnip3 and Bnip3L/Nix, leads to prominent relocalization of endolysosomes into inner mitochondrial compartments, in a manner independent of mitophagy. (elsevier.com)
  • However, the complexity of death receptor signalling has increased substantially during recent years. (mdpi.com)
  • In this review, we will summarise the current concepts of death receptor trafficking and its implications on receptor-associated signalling events. (mdpi.com)
  • Fas cell surface death receptor (FAS)-mediated apoptosis in spinal cord injury is reported to require mitochondrial signalling and the inhibition of FAS ligand (FASL) protects the cells from undergoing apoptosis [13]. (termedia.pl)
  • The extrinsic pathway involves engagement of particular "death" receptors that belong to the tumor TNFR (Tumor Necrosis Factor Receptor) family and, through the formation of the DISC (Death-Inducing-Signaling-Complex), leads to a cascade of activation of caspases, including Caspase8 and Caspase3, which in turn induce apoptosis. (thermofisher.com)
  • The most common death receptors involved in extrinsic apoptosis are Fas, DR5 (Death Receptor-5), and PERP. (thermofisher.com)
  • The cell-surface receptor Fas (CD95/Apo-1), a member of the TNFR family of receptors, is a key component of the extrinsic death pathway. (thermofisher.com)
  • The second member of this receptor family that is induced by p53 is DR5/Killer, the death-domain-containing receptor for TRAIL (TNF-Related Apoptosis-Inducing Ligand). (thermofisher.com)
  • SAHA down-regulated the expression of the apoptosis inhibitors FLIP and cIAP-2 and sensitized tumor cells to cytotoxic chemotherapy and death receptor activation. (aacrjournals.org)
  • Upon ensuing ''[[death domain]]'' (DD) aggregation, the receptor complex is internalized via the cellular endosomal machinery. (wikidoc.org)
  • The BH3-only protein Bid is known as a critical mediator of the mitochondrial pathway of apoptosis following death receptor activation. (elsevier.com)
  • Previously, we have demonstrated that Bim plays a prominent role in T cell shutdown in persistent infection by cooperating with the death receptor Fas, which regulates apoptosis in response to repeated TCR signaling. (jimmunol.org)
  • In mammals, two pathways of apoptosis, the "Bcl-2-regulated" (also called "intrinsic" or "mitochondrial") and the "death receptor"-induced (also called "extrinsic") synergistically regulate the shutdown of CD8 + T cell responses after a chronic immune response ( 4 , 5 ). (jimmunol.org)
  • In chronic immune responses elicited by persistent pathogens or tissue self-antigens, the "death receptor" (Fas ligand [FasL]) and the "Bcl-2-regulated" (Bim) pathways collaborate in effecting the removal of Ag-activated CD8 + T cells ( 12 - 14 ). (jimmunol.org)
  • In this setting, the death receptor pathway is thought to be triggered by repeated TCR ligation-mediated induction of FasL, leading to autocrine and/or paracrine Fas stimulation, whereas Bim may be induced in response to a decline in cytokine levels or repeated TCR stimulation-induced calcium flux ( 5 , 15 , 16 ). (jimmunol.org)
  • BMPR-1A(Bone Morphogenetic protein Receptor-1A) dz? (bioon.com.cn)
  • The use of BH3 mimetics, mimicking pro-apoptotic activator or sensitizer proteins of the intrinsic apoptotic pathway, is therefore a promising treatment strategy. (frontiersin.org)
  • Key regulators of the intrinsic apoptotic pathway are proteins of the B-cell lymphoma 2 (Bcl-2) family ( Youle and Strasser, 2008 ). (frontiersin.org)
  • Using a panel of 18 lymphoma cell lines, we show that a strategy we have developed, BH3 profiling, can identify apoptotic defects in cancer cells and separate them into three main classes based on position in the apoptotic pathway. (nih.gov)
  • The extrinsic pathway activates caspases via cell-surface death receptors, which respond to cognate death ligands expressed on immune-effector cells. (jci.org)
  • We demonstrated a notable ability of cisplatin or LA-12 to enhance the sensitivity of several human prostate cancer cell lines to TRAIL-induced cell death via an engagement of mitochondrial apoptotic pathway. (bireme.br)
  • Adverse outcome pathway development from protein alkylation to liver fibrosis. (wikipathways.org)
  • In this review, we reconnoitre the two major pathways (intrinsic and extrinsic) targeted cancer therapeutics, steering toward chief modulators of these pathways, such as B-cell lymphoma 2 protein family members (pro- and antiapoptotic), inhibitor of apoptosis proteins, and the foremost thespian of extrinsic pathway regulator, tumour necrosis factor-related apoptosis-inducing agent. (nature.com)
  • TNF-R1 activates Acid sphingomyelinase via pathway, which require TNFRSF1A-associated via death domain ( TRADD )/ Fas (TNFRSF6)-associated via death domain ( FADD ) adaptor proteins [ 5 ], [ 6 ]. (bio-rad.com)
  • Ceramide produced by Neutral sphingomyelinase stimulates Ceramides -activated Mitogen-activated protein kinase 1 and 3 ( ERK1/2 ) cascade and Acid sphingomyelinase may couple the TNF-R1 to the secretary pathway and to apoptosis via Cathepsin D [ 6 ]. (bio-rad.com)
  • Binding of death receptors (Fas, TNF-R, TRAIL-R) to their ligands (Fas-L, TNF, TRAIL) initiates the extrinsic apoptotic pathway. (nih.gov)
  • BH3-only proteins function at a proximal point in a conserved cell death pathway by binding, through their BH3 domains, to other Bcl-2 family members and triggering mitochondrial events associated with apoptosis. (pnas.org)
  • Biochemical and genetic evidence indicates that BH3-only proteins function at a point upstream of Bcl-2 in a cell death pathway conserved in both vertebrates and invertebrates ( 4 , 5 ). (pnas.org)
  • In Caenorhabditis elegans , the BH3-only protein Egl-1 operates at the most proximal point in a genetically defined pathway required for all programmed cell deaths ( 9 ). (pnas.org)
  • There is a remarkable degree of structural and functional conservation between the genes that control the cell death pathway in nematodes and mammals ( 5 ). (pnas.org)
  • Potentially, the identification of such genes would be important for delineating how diverse, seemingly unrelated apoptotic stimuli connect to a common cell death pathway in mammalian cells. (pnas.org)
  • For the first time, we revealed that ciglitazone is able to decrease E6 viral oncoprotein expression known to block TRAIL pathway and this was associated with cell death. (oncotarget.com)
  • Apoptosis can therefore occur either through an intrinsic pathway, in which signals from within the cell activate the process, or through an extrinsic pathway where death signals from outside the cell are received and processed by the cell to activate apoptosis. (scientificamerican.com)
  • Apoptosis regulators also include death receptors on the cell surface which bind to death signaling molecules, as part of the extrinsic apoptotic pathway. (scientificamerican.com)
  • The apoptotic signaling pathway regulated by TRAIL is initiated by its binding to agonist death receptors, namely DR4/TRAIL-R1 and DR5/TRAIL-R2. (spandidos-publications.com)
  • The direct cleavage of caspases ( 2 ), disruption of nuclear-cytoplasmic trafficking ( 3 , 4 ), relocalization of proapoptotic proteins ( 5 , 6 ), and cleavage of essential apoptotic adaptor proteins ( 7 , 8 ) have all been shown to occur as a result of action of Picornavirus protease activity and together suggest mechanisms by which picornaviruses can alter host cell apoptotic death pathways. (asm.org)
  • The single open reading frame of the genome is translated into a large polyprotein that undergoes posttranslational processing ( cis and trans cleavage) by the virally encoded proteases to yield mature, structural or nonstructural proteins ( 14 ). (asm.org)
  • Apoptosis, or programmed cell death, is mediated by the activation of caspases (Casp), a family of cysteine proteases present as proenzymes in all cells and activated by cleavage and reorganization of their subunits after an intracellular or extracellular apoptotic signal ( Nicholson, 1999 ). (jneurosci.org)
  • Activation of this executioner enzyme is irreversible, and results in the cleavage of numerous structural and functional proteins (e.g. (psu.edu)
  • Importantly, despite the presence of an intact BH3 domain, a tBid mutant lacking the mitochondrial targeting helices (α6 and α7) showed diminished apoptotic activity. (elsevier.com)
  • Altogether more than 700 proteins were analyzed representing all major types of protein families, i.e. protein receptors, kinases, phosphatases, transcription factors, and nuclear receptors. (mcponline.org)
  • Death receptors were initially recognised as potent inducers of apoptotic cell death and soon ambitious attempts were made to exploit selective ignition of controlled cellular suicide as therapeutic strategy in malignant diseases. (mdpi.com)
  • At the time of discovery, a subgroup of the TNFRSF, the so-called death receptors (DR), attracted considerable interest as robust cell-death induction upon ligand binding was recognised and triggered the ambitious goal for exploitation in therapeutic settings such as cancer therapy. (mdpi.com)
  • The aim of this work was to examine whether a fusion of BID with TAT cell penetrating peptide (TAT-BID) may be used for controlled sensitization of cancer cells to anticancer agents acting through death receptors (TRAIL) or DNA damage (camptothecin). (biomedcentral.com)
  • The level of BID is critical for viability of numerous cells because its silencing makes them resistant to apoptosis induced by death receptors ligands, e.g. (biomedcentral.com)
  • The mechanism by which the tumor cell gains resistance to TRAIL mainly include i) a deficiency of DR expression, ii) overexpression of anti-apoptotic proteins, or iii) competition of the decoy receptors (DcR1/TRAIL-R3 and DcR2/TRAIL-R4) for TRAIL binding ( 13 - 15 ). (spandidos-publications.com)
  • Our previous genome-wide gene expression analysis revealed that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptors 4 (DR4) and 5 (DR5) are markedly upregulated by the ethanolic extract of D. sohia seeds (EEDS) in A549 TRAIL-refractory cancer cells. (biomedcentral.com)
  • In the present study, we investigated whether the EEDS-mediated upregulation of TRAIL death receptors was associated with increased TRAIL-mediated toxicity in A549 cells in vitro. (biomedcentral.com)
  • EEDS can sensitize A549 cells to TRAIL cytotoxicity by upregulation of TRAIL death receptors. (biomedcentral.com)
  • Cyclin-dependent kinase 2 inhibitor SU9516 increases sensitivity of colorectal carcinoma cells Caco-2 but not HT29 to BH3 mimetic ABT-737. (bireme.br)
  • The aim of presented study was to determine the effect of ABT-737 inhibitor of anti-apoptotic proteins Bcl-2, Bcl-XL and Bcl-w as well as cyclin-dependent kinase 2 (CDK2) inhibitor SU9516 alone and in combination with ABT-737 on survival of colorectal cell lines HT29 and Caco-2. (bireme.br)
  • This inhibition depends on protein phosphatase 2 ( PP2A )-mediated dephosphorylation and by blocking AKT(PKB) translocation to plasma membrane via Protein kinase C zeta ( PKC-zeta ). (bio-rad.com)
  • In addition, in apigenin‑treated A375P cells, phosphorylated (p)‑p38 was upregulated and p‑extracellular signal‑regulated kinase (ERK), p‑c‑Jun N‑terminal kinase (JNK) and p‑protein kinase B (Akt) were downregulated. (spandidos-publications.com)
  • Overall, the findings of the present study indicated that apigenin attenuated the growth of A375SM melanoma cells by inducing apoptosis via regulating the Akt and mitogen‑activated protein kinase signaling pathways. (spandidos-publications.com)
  • p53 phosphorylation is mediated by several cellular kinases, including Chks (Checkpoint Kinases), CSNK1-Delta (Casein Kinase-1-Delta), CSNK2 (Casein Kinase-2), PKA (Protein Kinase A), CDK7 (Cyclin-Dependent Kinase-7), DNA-PK (DNA-Activated Protein Kinase), HIPK2 (Homeodomain-Interacting Protein Kinase-2), and JNK (Jun NH2-terminal kinase). (thermofisher.com)
  • Dedicator of Cytokinesis 2 -- Hiroshi Nishihara -- Domain Protein -- Dopamine and Adenosine 3',5'-Monophosphate-Regulated Phosphoprotein, 32 kDa -- Dopamine and cAMP-Regulated Phosphoprotein -- Dopamine- and cAMP-Regulated Phosphoprotein, Mr32 kDa -- Double-Stranded RNA-Activated Protein Kinase -- Down Syndrome Candidate Region 1 (DSCR1) -- Down Syndrome Critical Region 1 (DSCR1) -- Drag1. (opal-libraries.org)
  • Antibody-based proteomics provides a powerful approach for the functional study of the human proteome involving the systematic generation of protein-specific affinity reagents. (mcponline.org)
  • We used this strategy to construct a comprehensive, antibody-based protein atlas for expression and localization profiles in 48 normal human tissues and 20 different cancers. (mcponline.org)
  • The challenge for antibody-based proteomics is to move from a conventional protein-by-protein approach into a high throughput mode to allow chromosome wide analysis ( 6 , 7 ). (mcponline.org)
  • Two strategies have been used to counter the effects of IL-18:IL-18 binding protein (IL-18BP), a naturally occurring protein, and a neutralizing IL-18 antibody. (springer.com)
  • Antibody pairs are available for a diverse set of applications such as ELISA, Western Blotting-Immunoprecipitation and Proximity Litigation Assays for the investigation of protein protein interaction. (antibodies-online.com)
  • Rabbit IgG polyclonal antibody for BH3-interacting domain death agonist(Bid) detection. (bosterbio.com)
  • Two distinct yet interconnected signaling pathways control apoptosis by activating a core intracellular machinery of death proteases called caspases. (jci.org)
  • Caspases orchestrate the organized death of the cell by cleaving a small but specific complement of protein substrates. (jneurosci.org)
  • Once formed, the apoptosome goes on to activate a group of proteins known as caspases. (scientificamerican.com)
  • ii) elevated expression of inhibitors of apoptosis proteins (IAPs) that reduce the level of the initiator and effector caspases [ 3 ], and (iii) phosphorylation of apoptotic proteins [ 4 , 5 ] that makes them inaccessible to signaling and eventually prevents apoptosis in cancer cells. (biomedcentral.com)
  • Overall, picornaviruses, via the action of virally encoded proteins, exercise intricate control over and subvert cell death pathways, specifically apoptosis, thereby allowing viral replication to continue. (asm.org)
  • In this minireview, we aim to review and discuss current literature on Picornavirus modulation of cell death pathways with a view to integrating diverse studies to form a rational informed model of Picornavirus disruption of apoptotic pathways. (asm.org)
  • Together, we also will have a look from clinical perspective to address the agents (drugs) and therapeutic strategies adopted to target these specific proteins/pathways that have entered clinical trials. (nature.com)
  • Modulation of various cell death pathways by curcumin. (nih.gov)
  • Conclusions: Pro-apoptotic proteins involved in both the intrinsic and extrinsic apoptotic pathways were increased significantly by TEGDMA. (umich.edu)
  • What pathways are this gene/protein implicaed in? (cancerindex.org)
  • Progress in the knowledge of the structure of many of the main molecular actors of the apoptotic signal transduction pathways has driven the design of synthetic peptides that in some cases can function as simplified versions of their parent proteins. (jove.com)
  • Other p53-regulated gene functions communicate with adjacent cells, repair the damaged DNA or set up positive and negative feedback loops that enhance or attenuate the functions of the p53 protein and integrate these stress responses with other signal transduction pathways. (genome.jp)
  • As a research student, I prepared protein samples for immunoblotting, and contributed to a project that is examining the therapeutic potential of blocking apoptotic pathways to develop novel antidepressant treatments. (visualcv.com)
  • The development of therapeutic approaches which can specifically restore the cellular death pathways inactivated by the viral oncoproteins, appears to be fundamental for the clinical treatment of HPV-induced cervical cancer. (oncotarget.com)
  • To divide and grow uncontrollably, a cancer cell not only has to hijack normal cellular growth pathways, but also evade cellular death pathways. (scientificamerican.com)
  • Expression of these anti-apoptotic proteins is regulated by gonadotropins (FSH and LH) and locally produced growth factors (IGF-I and EGF family ligands) via cell survival signaling pathways. (psu.edu)
  • The absence of sufficient anti-apoptotic protein expression (dotted green lines) is proposed to tip the balance in favor of activating pro-apoptotic pathways (solid red lines). (psu.edu)
  • The acquired resistance of PC cells to current treatment protocols has been traced to apoptosis resistance based on the upregulation of anti-apoptotic proteins of the Bcl-2 family. (frontiersin.org)
  • According to their function in the apoptosis network, Bcl-2 family members can be divided into two different subgroups: the anti-apoptotic proteins (Bcl-2, Bcl-w, Bcl-xl, and Mcl-1) and the pro-apoptotic proteins. (frontiersin.org)
  • Structural analyses showed that the anti-apoptotic proteins share four regions of sequence homology dubbed Bcl-2 homology domains (BH1-4). (frontiersin.org)
  • (A) The effector proteins of the Bcl-2 family, Bax and Bak, are inhibited by the anti-apoptotic proteins Bcl-2, Bcl-w, Bcl-xl, and Mcl-1. (frontiersin.org)
  • Upon induction of apoptosis, the sensitizers BAD and NOXA inhibit the anti-apoptotic proteins. (frontiersin.org)
  • The activators BID, BIM, and PUMA can also block the anti-apoptotic proteins and can interact directly with Bax and Bak. (frontiersin.org)
  • They can be divided into pan-BH3 mimetics [GX15-070, (-)-gossypol, BI-97CI] antagonizing all members of the anti-apoptotic proteins, and specific BH3 mimetics (ABT-263/737), binding to Bcl-2, Bcl-xl, and Bcl-w, but not Mcl-1. (frontiersin.org)
  • In adults, protein changes were generally suggestive of a neurotrophic and neuroprotective effect of paroxetine, with significant downregulation of apoptotic proteins Galectin 7 and Cathepsin B, and upregulation of the neurotrophic factor Neurogenin 1 and the antioxidant proteins Aldose reductase and Carbonyl reductase 3. (frontiersin.org)
  • Colorectal carcinoma (CRC) that represents one of the major causes for cancer-related death in humans is often associated with over-expression of anti-apoptotic proteins of Bcl-2 family. (bireme.br)
  • Therefore, the purpose of this study was to determine the apoptotic proteins enhanced or suppressed during TEGDMA-induced apoptosis. (umich.edu)
  • Human apoptosis arrays were utilized to detect the relative levels of 43 apoptotic proteins. (umich.edu)
  • Some anti-apoptotic proteins were also altered. (umich.edu)
  • Interestingly, activation of HIF-1α and FAS converge in the release of pro-apoptotic proteins, but they are independent mechanisms. (termedia.pl)
  • These molecules are contributing to a better understanding of the activity and regulation of apoptotic proteins and also are setting the basis for the discovery of effective drugs to combat important diseases related to apoptosis. (jove.com)
  • Bcl-2, Bcl-XL, Bcl-W, Mcl-1 and A1 proteins function as anti-apoptotic proteins that inhibit apoptosis, while Bax, Bad, Bid, Bok, Bik and Bak (I swear these names are not made up! (scientificamerican.com)
  • are pro-apoptotic proteins that trigger apoptosis when activated. (scientificamerican.com)
  • The anti-apoptotic proteins bind to and inactivate the pro-apoptotic proteins in a healthy cell that does not need to die. (scientificamerican.com)
  • A common reason is reduction of the "functional dose" of apoptotic proteins [ 1 ], i.e. decrease of effective concentration of active proteins below a critical level necessary to carry out the process. (biomedcentral.com)
  • Bax is believed to interact with, and induce the opening of the mitochondrial voltage-dependent anion channel, VDAC . (wn.com)
  • We assess current developments in treatment that focus on mimicking the function of the BH3-only proteins to induce apoptosis, and consider their applicability to restore normal apoptotic responses in anchorage-independent disseminating tumor cells. (biologists.org)
  • This agent has been shown to induce death of advanced-stage melanoma cell lines 3- to 5-fold more effectively than normal cells and has led to a 60% decrease in tumor burden compared with control vehicle-treated animals. (aacrjournals.org)
  • Although activation of TLR signaling has been shown to induce apoptosis in cell lines [ 11 , 12 ], little is known about TLR involvement in cell death of primary brain cells. (biomedcentral.com)
  • How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? (semanticscholar.org)
  • Furthermore, the knockdown of Sp1 protein by Sp1-specific inhibitor, mithramycin A, and siRNA resulted in the alteration of truncated Bid and Bim to induce apoptosis. (elsevier.com)
  • Intrinsic apoptosis involves BH3-only protein activation of Bax/Bak-mediated mitochondrial outer membrane permeabilization (MOMP). (elsevier.com)
  • Dendra2 has been successfully fused to a variety of proteins including cytoplasmic beta-actin, BH3 interacting domain death agonist (BID), nucleolar protein fibrillarin, vimentin, and alpha-tubulin. (clontech.com)
  • This class of proteins, which includes bcl-2-interacting killer (Bik), bcl-x L /bcl-2-associated death promoter (Bad), BH3-interacting domain death agonist (Bid), Bcl-2-interacting mediator of cell death (Bim), egg-laying-defective-1 (Egl-1), and harakiri (Hrk), uses BH3 for binding to anti-apoptotic members of the Bcl-2 family and for inducing apoptosis ( 4 ). (pnas.org)
  • In an acute immune response, cessation of lymphocyte recruitment and proliferation is thought to be triggered by a decline in cytokine levels and is mediated (largely) through activation of the BH3-only proteins Bcl-2 interacting mediator of cell death (Bim) and p53 upregulated modulator of apoptosis (Puma) ( 6 - 9 ). (jimmunol.org)
  • The encoded protein is a member of the BCL-2 family of cell death regulators. (genecards.org)
  • Bcl-2 proteins act as anti- or pro- apoptotic regulators that are involved in a wide variety of cellular activities. (wn.com)
  • The primary regulators of apoptosis are proteins belonging to a group known as the Bcl-2 family. (scientificamerican.com)
  • We show that the nonstructural HCV viral protein NS5A is sufficient to activate a calpain cysteine protease, leading to degradation of Bid. (cnrs.fr)
  • Dendra2 is an ideal tool for real-time tracking protein dynamics (movement, degradation, etc.) and monitoring selective cell fate. (clontech.com)
  • Visualizing real-time protein dynamics (movement, degradation, etc. (clontech.com)
  • or heterogeneous chains in which different ubiquitin-ubiquitin linkages are found, have also been reported to target proteins for proteasomal degradation. (biologists.org)
  • Linear chains, in which the ubiquitin links are attached to one another 'head-to-tail', and heterologous chains, in which the links are made of ubiquitin and a ubiquitin-like protein, such as small ubiquitin-like modifier (SUMO), have additionally been shown to target proteins for proteasomal degradation. (biologists.org)
  • HPV E6 protein binds to p53 and favours its degradation by the proteasome through the formation of a complex with E6-associated protein (E6AP), a member of the E3-ubiquitin ligase family. (oncotarget.com)
  • HPV E7 protein interacts with pRb, inducing its proteolytic degradation leading to the destabilization and the disruption of Rb/E2F repressor complexes which results in increased transcription of E2F-responsive genes and S-phase cell cycle progression [ 4 ]. (oncotarget.com)
  • Ky2 markedly decreased the level of Sp1 protein expression through both the decrease of Sp1 mRNA level and proteasome-dependent protein degradation. (elsevier.com)
  • PERP is a putative tetraspan transmembrane protein that represents a new member of the PMP-22/Gas family of proteins implicated in cell growth regulation. (thermofisher.com)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a type II transmembrane protein belonging to the tumor necrosis factor (TNF) superfamily. (spandidos-publications.com)
  • Surprisingly, this protein has been reported to be targetted to the outer mitochondrial membrane ( Gutiérrez-Aguilar and Baines, 2013 ). (tcdb.org)
  • In response to apoptotic signaling, BID interacts with another Bcl-2 family protein , Bax , leading to the insertion of Bax into organelle membranes, primarily the outer mitochondrial membrane. (wn.com)
  • BID is a member of the Bcl-2 family of proteins that regulates outer mitochondrial membrane permeability. (rndsystems.com)
  • This latter group of BH3-only proteins can bind to the prosurvival Bcl-2 family members thereby removing the inhibition of Bax and Bak and inducing apoptosis by permeabilizing the outer mitochondrial membrane ( 2 , 3 ). (jimmunol.org)
  • The Bcl-2 family proteins regulate the cellular response to apoptotic stimuli ( 1 , 2 ). (pnas.org)
  • These proteases are essential for viral polyprotein processing and also cleave cellular proteins. (asm.org)
  • Despite dimerization capacity, JRed demonstrates successful performance in fusions with subcellular localization signals and many cellular proteins including BH3 interacting domain death agonist (BID), nucleolar protein fibrillarin, dopamin transporter (hDAT). (evrogen.com)
  • Expression changes of cellular proteins were determined by western blot analysis. (biomedcentral.com)
  • The anti-apoptotic Bcl-2 proteins, including Bcl-2 itself, can bind BID and inhibit BID's ability to activate Bax. (wikipedia.org)
  • As a result, the anti-apoptotic Bcl-2 proteins may inhibit apoptosis by sequestering BID, leading to reduced Bax activation. (wikipedia.org)
  • Mechanism of apoptosis induction by inhibition of the anti-apoptotic BCL-2 proteins. (semanticscholar.org)
  • Koga H, Hayashi K, Taketomi E et al (1996) Restriction fragment length polymorphism of genes of the alpha 2(XI) collagen, bone morphogenetic protein-2, alkaline phosphatase, and tumor necrosis factor-alpha among patients with ossification of posterior longitudinal ligament and controls from the Japanese population. (springer.com)
  • The p53 protein is a transcription factor that, when activated as part of the cell's response to stress, regulates many downstream target genes, including BID. (wikipedia.org)
  • Moreover, disregulation of the mechanisms that control transcription of BH3-only genes in this class may contribute to defects in apoptosis in diseases such as cancer. (pnas.org)
  • Tumor protein p53 is a nuclear transcription factor that regulates the expression of a wide variety of genes involved in apoptosis, growth arrest, or senescence in response to genotoxic or cellular stress. (thermofisher.com)
  • In doing so, it activates expression of downstream genes leading to programmed cell death and/or cell cycle arrest, thus functioning as a tumor suppressor. (thermofisher.com)
  • The p53 protein is employed as a transcriptional activator of p53-regulated genes. (genome.jp)
  • Adolescent rats failed to show the neurotrophic and neuroprotective effects observed in adults, instead displaying upregulation of the proapoptotic protein BH3-interacting domain death agonist (4.3-fold). (frontiersin.org)
  • Binds the BH3-interacting domain death agonist, BID. (tcdb.org)
  • Egl-1 binds to the nematode Bcl-2 counterpart, Ced-9, and antagonizes its function, similar to the function ascribed to mammalian BH3 proteins. (pnas.org)
  • A member of the Bcl-2 protein family that reversibly binds MEMBRANES. (bvsalud.org)
  • Bcl-2 family members share one or more of the four characteristic domains of homology entitled the Bcl-2 homology (BH) domains (named BH1, BH2, BH3 and BH4), and can form hetero- or homodimers. (wn.com)
  • Members of this family can function to either suppress or promote cell death, and are characterized by the presence of up to four conserved amino acid motifs, termed Bcl-2 homology (BH) domains ( 1 , 2 ). (pnas.org)
  • The antiapoptotic proteins (Bcl-2, Bcl-X L , Bcl-W, A1, and Mcl-1) share sequence homology in their Bcl-2 homology (BH) domains. (jimmunol.org)
  • Isoform 2 is expressed in spleen, pancreas and placenta (at protein level). (antibodyplus.com)
  • Isoform 3 is expressed in lung, pancreas and spleen (at protein level). (antibodyplus.com)
  • The present review gives an overview of preclinical and clinical studies with pan- and specific BH3 mimetics as sensitizers for cell death and gives an outlook how they could be effectively used for the therapy of advanced PC in future. (frontiersin.org)
  • Importantly, we newly demonstrated LA-12-mediated enhancement of TRAIL-induced cell death in cancer cells derived from human patient prostate tumor specimens. (bireme.br)
  • Expressed proteins were purified from cell lysates using 96-well glutathione-affinity plates and quantitated on a Caliper LabChip 90 (LC90) instrument. (thermofisher.com)
  • Recent work has suggested that secreting, mammary epithelial cells (MECs) have another function to perform before they undergo cell death in the involuting mammary gland. (springer.com)
  • In bladder cancer cells, regardless of H-RAS mutational status, at clinically achievable doses, PDE5 inhibitors interacted in a greater than additive fashion with doxorubicin/mitomycin C/gemcitabine/cisplatin/paclitaxel to cause cell death. (aspetjournals.org)
  • In pancreatic tumor cells expressing mutant active K-RAS, PDE5 inhibitors interacted in a greater than additive fashion with doxorubicin/gemcitabine/paclitaxel to cause cell death. (aspetjournals.org)
  • As viruses require a viable cell for replication, the death of the cell limits cellular functions that are required for virus replication and propagation. (asm.org)
  • The viral proteases not only participate in the maturation of the viral proteins but also act against cellular factors, resulting in host cell shutoff and increased virus replication. (asm.org)
  • Cell death is an important cellular mechanism to limit viral spread, and viruses, including picornaviruses, have evolved to inhibit cell death. (asm.org)
  • Cell death can occur as a result of many stimuli with the type of stimulus determining the type of cell death. (asm.org)
  • Apoptosis is a process of selective, controlled cell death ( 15 - 17 ), which utilizes a cascade of signaling proteins after the activation of a death signal. (asm.org)
  • Owing to the fact that apoptosis causes minimal inflammation and damage to the tissue, apoptotic cell death-based therapy has been the centre of attraction for the development of anticancer drugs. (nature.com)
  • Apoptosis or known as programmed cell death is a physiological process that is responsible for eliminating unwanted, damaged, mutated and/or aged cells that might pose robust threat to the living body if not removed. (nature.com)
  • Cell death is essential for life. (nature.com)
  • 1 Cell death plays critical roles in regulating embryonic development, maintaining tissue homoeostasis, controlling immune function, tumour suppression and infection resistance. (nature.com)
  • 3 Cell death is responsible for an array of dispensable physiological processes, including removal of useless cells from the immune system, 6 duct formation in mammary glands, thymus degeneration with ageing and finally elimination of infected cells to limit pathogen spread. (nature.com)
  • Cell Death and Differentiation , 21 (12), 1862-1876. (elsevier.com)
  • Differentiation of monocytes towards a macrophage phenotype is also accompanied by an increase of resistance against various apoptotic stimuli, a required characteristic that allows macrophages to accomplish their function in a stressful environment.Apoptosis, a form of programmed cell death, is a tightly regulated process, needed to maintain homeostasis by balancing proliferation with cellular demise. (nih.gov)
  • Cell Death Differ. (wikipedia.org)
  • Description: A sandwich quantitative ELISA assay kit for detection of Mouse BH3 Interacting Domain Death Agonist (Bid) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (ksiazkiwnauce.pl)
  • In all cases, supernumerary cells in the forebrain and midbrain cause neural tissue protrusions through the skull as a result of defects in apoptotic cell death. (jneurosci.org)
  • The release of these monomers causes a variety of reactions that can lead to cell death. (umich.edu)
  • This cell death can be either necrotic that is characterized mainly by inflammation and injury to the surrounding tissues, or apoptotic that elicits little inflammatory responses, if any at all. (umich.edu)
  • Cell lysates were then prepared and the protein concentrations determined using the Bradford protein assay. (umich.edu)
  • However, especially during recent years it has become obvious that DR signalling is far more than cell death induction. (mdpi.com)
  • Mammary gland development goes through different stages that depend on proper regulation of proliferation and programmed cell death (apoptosis) ( Fig. 1 A). Sex hormone-dependent cyclic organization of growth and survival provides the plasticity of the mammary gland that is needed for its function. (biologists.org)
  • Hence, failure to maintain a proper balance between cell expansion and cell death is key to the neoplastic growth of mammary tissues. (biologists.org)
  • however, the molecular mechanisms leading to leelamine-mediated cell death have not been identified. (aacrjournals.org)
  • Furthermore, target cells in which BID (BH3-interacting domain death agonist) expression was inhibited also remained highly susceptible to NK cell-mediated killing, revealing redundancy in the pro-apoptotic response to human cytotoxic lymphocytes. (portlandpress.com)
  • Zhang G, Zha J, Liu J, Di J. Minocycline impedes mitochondrial-dependent cell death and stabilizes expression of hypoxia inducible factor-1α in spinal cord injury. (termedia.pl)
  • Traumatic spinal cord injury includes a complex pattern of pathophysiological processes out of which mitochondrial activity in cell survival and death holds a greater impact [5]. (termedia.pl)
  • Minocycline's efficacy to impede mitochondrial cell death has been established previously [6, 7]. (termedia.pl)
  • Another important mitochondrial target gene is HIF-1α, and the expression of HIF-1α is time dependent, leading to cell death or cell survival following neuronal injury [14]. (termedia.pl)
  • In this study, we hypothesised that minocycline modulates mitochondrial cell death via mechanisms interlinking HIF-1α stabilization and FASL-mediated apoptosis. (termedia.pl)
  • Given that CHOP is implicated in ER stress associated cell death, the intracellular GSH concentration may direct cell fate in response to ER stress. (ufl.edu)
  • Three imaging based techniques (live cell imaging, immunofluorescence (IF)/immunocytochemistry (ICC) and immunohistochemistry (IHC)) present the ability to gather useful information about apoptosis through visualization of key proteins. (bio-rad-antibodies.com)
  • It can even be used to differentiate between apoptosis and another type of cell death, necrosis. (bio-rad-antibodies.com)
  • These results suggest that the transcriptional regulation of bbc3 contributes to the transduction of diverse cell death and survival signals. (pnas.org)
  • The function of BH3 as a cell death domain has been further revealed by an emerging group of "BH3-only" proteins, which share only BH3 in common with other Bcl-2 family members. (pnas.org)
  • The functions of the BH3 proteins Bad and Bid are regulated by phosphorylation and proteolytic activation, respectively, in response to extrinsic cell survival/cell death stimuli ( 6 - 8 ). (pnas.org)
  • The essential contribution of Egl-1 and its transcriptional regulation to programmed cell death in C. elegans strongly implies that apoptosis in mammalian cells may depend on the transcriptional control of gene(s) encoding BH3-only proteins. (pnas.org)
  • Apoptosis is known to play a role in cell death in transient retinal ischemia. (arvojournals.org)
  • Apoptosis is a genetically controlled mechanism of cell death that is essential for the elimination of unwanted cells during normal development and for the maintenance of tissue homeostasis. (thermofisher.com)
  • DR5 is induced by p53 in response to DNA damage and in turn promotes cell death through Caspase8. (thermofisher.com)
  • Transfection of Bcl-2 cDNA partially suppressed SAHA-induced cell death. (aacrjournals.org)
  • Pubmed ID: 12450324 Apoptosis is a complex process that plays a central role in physiological and pathological cell death. (jove.com)
  • This trimerization usually leads to apoptosis, or cell death. (wikidoc.org)
  • Cell signaling == Fas forms the [[death-inducing signaling complex]] (DISC) upon ligand binding. (wikidoc.org)
  • Following this cytokine burst, microglial cells rapidly undergo cell death by apoptosis. (biomedcentral.com)
  • We hypothesized that TLR2 signaling might mediate the cell death process as well. (biomedcentral.com)
  • To test this hypothesis, we investigated HSV-induced cell death of microglia obtained from both wild-type and TLR2 -/- mice. (biomedcentral.com)
  • Cell death was studied by oligonucleosomal ELISA and TUNEL staining, and the mechanisms of apoptosis were further analyzed using murine apoptosis-specific microarrays. (biomedcentral.com)
  • HSV infection induced apoptotic cell death in microglial cells from wild-type as well as TLR2 cells. (biomedcentral.com)
  • However, the cell death at 24 h p.i. was markedly lower in knockout cells. (biomedcentral.com)
  • It is a highly specific process that is time- (e.g. cell cycle), compartment- (e.g. nucleus or endoplasmic reticulum) and substrate quality- (e.g. denatured or misfolded proteins) dependent, and allows fast adaptation to changing conditions. (biologists.org)
  • it is cell death. (scientificamerican.com)
  • But before I explain how cancer cells do this, we need to understand how the process of cellular death occurs in a normal cell. (scientificamerican.com)
  • When microinjected into cells, these anti-VDAC antibodies, but not control antibodies, also prevented Bax-induced cytochrome c release and apoptosis, whereas the antibodies did not prevent Bid-induced apoptosis, indicating that the VDAC is essential for Bax-induced, but not Bid-induced, apoptogenic mitochondrial changes and apoptotic cell death. (nih.gov)
  • Apoptotic cell death was monitored by western blot analysis. (biomedcentral.com)
  • Co-treatment of A549 cells with sub-lethal dose of EEDS and recombinant TRAIL increased the apoptotic cell death. (biomedcentral.com)
  • In this study, we investigated the contribution of the BH3-only family protein Bid in the shutdown of T cell responses after acute and persistent infection. (jimmunol.org)
  • The study enabled the identification of over 2000 proteins and 153 cancer markers, and revealed for the first time that the G1-stage of the cell cycle is not only a rich source of cancer markers, but also a host to an intricate network of functional relationships within the majority of these markers. (biomedcentral.com)
  • Key to its regulation is the phosphorylation of the retinoblastoma protein (pRb or RB1) by active cyclin D-CDK4/6 and cyclin E-CDK2 complexes in early and late G1, respectively, an event that results in the release of E2F transcription factors that signal the cell to continue into the S-phase, replicate and proliferate. (biomedcentral.com)
  • This allows the adaptor molecule ''Fas-associated death domain'' (FADD) to bind the death domain of Fas through its own death domain. (wikidoc.org)
  • Accordingly, the current study examined changes in hippocampal protein expression following chronic administration of paroxetine in drinking water (target dose = 10 mg/kg for 22 days) to adult and adolescent rats. (frontiersin.org)
  • Results indicated age-specific changes in protein expression, with paroxetine significantly altering expression of 8 proteins in adolescents only and 10 proteins solely in adults. (frontiersin.org)
  • Instead of this, we have shown that treatment of HT29 cells with SU9516 is associated with decreased expression of tumour suppressor protein p53. (bireme.br)
  • Our findings provide a rationale for clinical use of Bcl-2 family inhibitors in combination with CDK2 inhibitors for treatment of Mcl-1-dependent colorectal tumours associated with expression of Bcl-2, Bcl-XL and Bcl-w proteins. (bireme.br)
  • The cDNA ORF of each gene was cloned into pDEST27 expression vector by Gateway cloning, which incorporates a GST tag to the N-terminal of each protein. (thermofisher.com)
  • Expression of cellular FLICE-like inhibitory protein-short did not significantly inhibit chemotherapy lethality but did significantly reduce enhanced killing in combination with sildenafil. (aspetjournals.org)
  • It is also possible to generate protein expression data on many different individual patients to evaluate heterogeneity of tissue profiles ( 2 , 3 ). (mcponline.org)
  • 8 ) showed that the combination of the cloning and expression of recombinant protein fragments with immunohistochemistry analysis could be used for systematic protein expression and subcellular localization describing distribution and expression of putative gene products in normal tissues as well as in common cancers and other forms of diseased tissues. (mcponline.org)
  • The use of tissue microarrays (TMAs) generated from multiple biopsies combined into single paraffin blocks enabled high throughput analysis of protein expression in various tissues and organs ( 2 ). (mcponline.org)
  • 10 ) showed that high throughput analysis of protein expression can be performed with a standard set of tissue microarrays representing both normal and cancer tissues. (mcponline.org)
  • We show that a comprehensive atlas of human protein expression patterns in normal and cancer tissues can be created by combining the methods mentioned above. (mcponline.org)
  • Transcription factor KAISO (POZ/BTB family protein, ZBTB33) expression is induced by genotoxic stress in a tumor suppressor p53-dependent manner. (pnas.org)
  • Scope includes mutations and abnormal protein expression. (cancerindex.org)
  • To show that palmitate induced ER stress, XBP1s mRNA expression and CHOP protein expression were measured. (ufl.edu)
  • mRNA expression of the ER chaperone Ero-1a was measured to evaluate the effects of palmitate and GSH treatment on protein folding. (ufl.edu)
  • Here, we describe a strongly pro-apoptotic BH3-only protein, designated Bbc3, whose expression increases in response to diverse apoptotic stimuli. (pnas.org)
  • The changes in the expression levels of apoptosis‑related proteins in A375P and A375SM melanoma cells were subsequently detected using western blot analysis. (spandidos-publications.com)
  • However, in A375SM cells, apigenin treatment increased p‑ERK and p‑JNK and decreased p‑p38 and p‑Akt protein expression levels. (spandidos-publications.com)
  • These protein expression changes induced by DCE were usually limited to the range ± 10%, suggesting murine hepatocytes were safely reactive to DCE within the threshold of physiological homeostasis. (springeropen.com)
  • Upregulation of DR5 by EEDS was mediated by an endoplasmic reticulum stress-induced transcription factor, CCAAT/enhancer-binding protein homologous protein (CHOP), and knockdown of CHOP expression inhibited EEDS-induced DR5 upregulation and abolished the EEDS-associated increase in TRAIL toxicity in A549 cells. (biomedcentral.com)
  • Several BH3 peptides relieved the inhibition of Bax caused by the antiapoptotic Bcl-x(L) and/or Mcl-1 proteins, some displaying a specificity for either Bcl-x(L) or Mcl-1. (nih.gov)
  • Should the Mouse BH3 Interacting Domain Death Agonist (Bid) ELISA Kit is proven to show malperformance, you will receive a refund or a free replacement. (ksiazkiwnauce.pl)
  • 9 ) showed that this strategy could be further improved by a streamlined approach for affinity purification of the antibodies to generate monospecific antibodies (msAbs) 1 and the subsequent validation of the specificity of these antibodies by protein microarrays. (mcponline.org)
  • For positive and negative control design, consult "Tissue specificity" under Protein Target Info . (bosterbio.com)
  • The identification of cancer marker regulatory components that act not alone, but within networks, represents an invaluable resource for elucidating the moxlecular mechanisms that govern the uncontrolled proliferation of cancer cells, as well as for catalyzing the development of protein panels with biomarker and drug target potential, screening tests with improved sensitivity and specificity, and novel cancer therapies aimed at pursuing multiple drug targets. (biomedcentral.com)
  • Three major clusters of interacting proteins emerged: (a) signaling, (b) DNA repair, and (c) oxidative phosphorylation. (biomedcentral.com)
  • These include chains anchored to residues other than internal lysine in the substrates, chains assembled through linking residues other than lysine 48 in ubiquitin, and mixed chains made of both ubiquitin and a ubiquitin-like protein. (biologists.org)
  • Furthermore, some proteins can be degraded following modification by a single ubiquitin (monoubiquitylation) or multiple single ubiquitins (multiple monoubiquitylation). (biologists.org)
  • also known as ubiquitin-conjugating enzyme, UBC) and a ubiquitin-protein ligase (E3). (biologists.org)
  • In general, modification by ubiquitin serves as a recognition element in trans, whereby different downstream effectors bind to the ubiquitin-modified protein to affect its fate and/or function. (biologists.org)
  • Picornavirus proteases cleave proapoptotic adaptor proteins, resulting in downregulation of apoptosis. (asm.org)
  • Furthermore, Bax activator molecules (cleaved Bid protein and the Bim BH3 peptide) synergistically induced cytochrome c release when introduced into cells along with derepressor BH3 peptides. (nih.gov)
  • Using a Bax-dependent membrane-permeabilization assay, we show that peptides corresponding to the BH3 domains of Bcl-2 family "BH3-only" proteins have dual functions. (nih.gov)
  • These observations support a unified model of BH3 domain function, encompassing both positive and negative regulation of other Bcl-2 family members. (nih.gov)
  • Schematic representation of the interactions between different members of the Bcl-2 protein family and BH3 mimetics. (frontiersin.org)
  • The BH3 interacting-domain death agonist , or BID , gene is a pro- apoptotic member of the Bcl-2 protein family. (wn.com)
  • The BH3-only subset of the Bcl-2 family of proteins contain only a single BH3-domain. (genenames.org)
  • The BH3-only family members are Bim, Bid, BAD and others. (genenames.org)
  • Intact BH3 motif is required by BIK, BID, BAK, BAD and BAX for their pro-apoptotic activity and for their interaction with anti-apoptotic members of the Bcl-2 family. (antibodyplus.com)
  • The BH3 domain-only protein, BID, a death agonist member of the Bcl-2/Bcl-xL family (1), is localized in the cytosolic fraction of cells as an inactive precursor (2,3). (antibodyplus.com)