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.
The motion of a liquid through a membrane (or plug or capillary) consequent upon the application of an electric field across the membrane. (Oxford Dictionary of Biochemistry and Molecular Biology, 2001)
A technique for maintenance or growth of animal organs in vitro. It refers to three-dimensional cultures of undisaggregated tissue retaining some or all of the histological features of the tissue in vivo. (Freshney, Culture of Animal Cells, 3d ed, p1)
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
Used as feed supplement for sheep and cattle since it is a good non-protein nitrogen source. In strongly alkaline solution biuret gives a violet color with copper sulfate.
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.
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.
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.
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.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
Immunoglobulins produced in response to VIRAL ANTIGENS.
Antibodies produced by a single clone of cells.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
A class of morphologically heterogeneous cytoplasmic particles in animal and plant tissues characterized by their content of hydrolytic enzymes and the structure-linked latency of these enzymes. The intracellular functions of lysosomes depend on their lytic potential. The single unit membrane of the lysosome acts as a barrier between the enzymes enclosed in the lysosome and the external substrate. The activity of the enzymes contained in lysosomes is limited or nil unless the vesicle in which they are enclosed is ruptured. Such rupture is supposed to be under metabolic (hormonal) control. (From Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
An inhibitor of apoptosis protein that is translated by a rare cap-independent mechanism. It blocks caspase-mediated cellular destruction by inhibiting CASPASE 3; CASPASE 7; and CASPASE 9.
Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.
A multi-domain mitochondrial membrane protein and member of the bcl-2 Protein family. Bak protein interacts with TUMOR SUPPRESSOR PROTEIN P53 and promotes APOPTOSIS.

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 ...
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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. ...
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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.. ...
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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.
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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...
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 ...
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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...
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...
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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...
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.
The SPCA has begun uplifting hordes of animals, birds and cats from a Northland farm after their owner lost a bid to appeal against
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.
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 ...
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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 ...
Our lab is cross-disciplinary, bringing together computational biology, protein design, and molecular biology approaches. We assess the structural bioinformatics of OMPs (outer membrane proteins) and apply the results to de novo OMP protein design and to native OMP manipulation.. OMPs are a ripe target for cancer therapeutics. Mitochondria have recently become a focus of cancer therapies due to the fact that mitochondrial outer membrane permeabilization leads to apoptosis or necrosis. We explore mitochondrial membrane permeabilization through manipulation of the OMP pores that already exist in the mitochondrial outer membrane. This may have pharmaceutical consequences because tumorigenic mitochondrial membranes can be selectively targeted in themselves as they have been shown to accumulate lipophilic cations.. Beyond this mechanistic understanding, knowledge of the relationship between OMP chemistry and structure will allow new OMPs to be designed for use in vaccines and will facilitate ...
Mtch1 (untagged) - Mouse mitochondrial carrier homolog 1 (C. elegans) (Mtch1), nuclear gene encoding mitochondrial protein, (10ug), 10 µg.
Homodimer. Forms higher oligomers under stress conditions. Interacts with BCL2L11. Interaction with BCL2L11 promotes BAX oligomerization and association with mitochondrial membranes, with subsequent release of cytochrome c. Forms heterodimers with BCL2, BCL2L1 isoform Bcl-X(L), BCL2L2, MCL1 and A1. Interacts with SH3GLB1 and HN. Interacts with SFN and YWHAZ; the interaction occurs in the cytoplasm. Under stress conditions, JNK-mediated phosphorylation of SFN and YWHAZ, releases BAX to mitochondria. Isoform Sigma interacts with BCL2A1 and BCL2L1 isoform Bcl-X(L). Interacts with RNF144B, which regulates the ubiquitin-dependent stability of BAX. Interacts with CLU under stress conditions that cause a conformation change leading to BAX oligomerization and association with mitochondria. Does not interact with CLU in unstressed cells. Interacts with FAIM2/LFG2. Interacts with RTL10/BOP. Interacts (via a C-terminal 33 residues) with NOL3 (via CARD domain); inhibits BAX activation and translocation and ...
The neighborhood itself has struggled to attract private businesses and office workers, in part because it lacks nearby services and retail. Service and retail providers in turn have had little incentive to open shop in Anacostia until more businesses and consumers are on the street. That conundrum is reflected in the embryonic BID formation. While corporations typically sponsor the BIDs that promote doing business in the neighborhood, that lack of commerce has hindered the Anacostia BIDs formation. Though landowners in the area point to much potential - a historic downtown, a Metro stop, the coming St. Elizabeths project - without a corporate base to fund the BID, lack of money has kept Anacostias promoter-in-chief from becoming a reality. That may be starting to change ...
Apoptosis is initiated when Bcl-2 and its prosurvival relatives are engaged by proapoptotic BH3-only proteins via interaction of its BH3 domain with a groove on the Bcl-2-like proteins ...
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.. ...
Senate Majority Leader Mitch McConnell (R-KY) hasnt kept quiet about his interest in Secretary of State Mike Pompeo launching a bid for the Kansas Senate seat…
Japans Dainippon Sumitomo Pharma Co Ltd(4506.T) plans to launch a bid to acquire Sepracor Inc SEPR.Ofor about 250 billion yen ($2.70 billion), the Nikkei businessdaily said.
The chairman of one of Chinas leading real estate investment groups Beijing Zhongkun, made famous by his $8.8 million bid to buy a 115 square mile farm in Iceland, says the deal would have been very profitable had it gone through.
A city council criticises a family for trying to lure back their missing dog by leaving a trail of their diluted urine on the street.
Trade is continuing to be largely steady among the Beltex here at Carlisle, but with some of the better pens coming in now some good prices have been achie
Begrippenlijst Spoorse Begrippen bedoeld voor taalexamen voor machinist, rangeerder, wagencontroleur en treindienstleider Bronvermelding: Business Information Document van ProRail, documentnummer BID00009,
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. ...
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 ...
... 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- ...
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) for ELISA, ICC/IF, IHC-P, WB. Anti-Bid pAb (GTX31689) is tested in Mouse samples. 100% Ab ... BH3 interacting domain death agonist. Background. This gene encodes a death agonist that heterodimerizes with either agonist ... The encoded protein is a member of the BCL-2 family of cell death regulators. It is a mediator of mitochondrial damage induced ... Cancer > Apoptosis > Induction > Death domain receptors. *Cancer > Apoptosis > Metastasis and Invasion > Metastasis > Lymphatic ...
BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Carrier Proteins; 9007-43-6 / Cytochromes c; EC 3.4. ... BH3 Interacting Domain Death Agonist Protein. Blotting, Western. Carrier Proteins / physiology. Caspase 3. Caspase 8. Caspase 9 ... Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 ... 22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; ...
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. ...
... thereby inducing cell death. Here we report that Bid is … ... BH3 Interacting Domain Death Agonist Protein * BID protein, ... thereby inducing cell death. Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). ... BH3 Interacting Domain Death Agonist Protein * Carrier Proteins / genetics * Carrier Proteins / metabolism* ...
... 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 ...
... is a pro-apoptotic protein involved in death receptor-induced and mitochondria-mediated apoptosis. Recently, it has also been ... is a pro-apoptotic protein involved in death receptor-induced and mitochondria-mediated apoptosis. Recently, it has also been ... The BH3 interacting-domain death agonist (BID) is a pro-apoptotic protein involved in death receptor-induced and mitochondria- ... The BH3 interacting-domain death agonist (BID) is a proapoptotic B-cell lymphoma-2 (BCL-2) family protein involved in death ...
Apoptosis Regulatory Proteins / genetics * Apoptosis Regulatory Proteins / metabolism* * BH3 Interacting Domain Death Agonist ... We identify B-cell-receptor-associated protein 31 (BAP31) as an interacting partner of CDIP1. Upon ER stress, CDIP1 is induced ... Intracellular Signaling Peptides and Proteins / antagonists & inhibitors * Intracellular Signaling Peptides and Proteins / ... Apoptosis Regulatory Proteins * BH3 Interacting Domain Death Agonist Protein * Bcap31 protein, mouse ...
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 ...
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 ...
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 ...
... 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 ...
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 ...
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 ...
... 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 ...
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. ...
... cancer cells 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 ...
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)
  • 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)
  • The BH3 interacting-domain death agonist (BID) is a pro-apoptotic protein involved in death receptor-induced and mitochondria-mediated apoptosis. (frontiersin.org)
  • The BH3 interacting-domain death agonist (BID) is a proapoptotic B-cell lymphoma-2 (BCL-2) family protein involved in death receptor-induced apoptosis. (frontiersin.org)
  • We identify B-cell-receptor-associated protein 31 (BAP31) as an interacting partner of CDIP1. (nih.gov)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • These ligand/receptor complexes recruit adaptor molecules, such as Fas-associated protein with death domain (FADD), on their death effector domains (DED), leading to the formation of Death-Inducing Signaling Complexes (DISC) that in turn recruit pro-caspase 8. (biomedcentral.com)
  • We commonly distinguish between two different types of apoptosis: the intrinsic pathway, mediated by mitochondria in response to internal stimuli such as DNA damage, and the extrinsic pathway, mediated by extracellular death receptors (for example, binding of FasL to the FasLG receptor) (Figure 1). (bioradiations.com)
  • Proteins with a type 1 peroxisomal targeting signal (PTS1) are bound by the import receptor Pex5p in the cytosol and guided to the peroxisomal membrane. (bioscirep.org)
  • The PTS1-receptor is either polyubiquitinated via peptide bonds at two certain lysines and results in proteasomal degradation or monoubiquitinated via a thioester-bond at a conserved cysteine, which enables the recycling of Pex5p and further rounds of matrix protein import. (bioscirep.org)
  • To this end, cargo proteins are equipped with a targeting sequence, either a C-terminal PTS1 (peroxisomal targeting signal type 1) or an N-terminal PTS2, which are recognized and bound by the import receptor Pex5p or Pex7p respectively [ 8 ]. (bioscirep.org)
  • Monoubiquitination primes the receptor for its export back to the cytosol to allow a new round of matrix protein import [ 12 , 14 , 15 ]. (bioscirep.org)
  • CASP8 cleaves this encoded protein, and the COOH-terminal part translocates to mitochondria where it tr. (genecards.org)
  • 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)
  • In these cells, following cleavage by caspase 8, the C-terminal fragment of Bid translocates to mitochondria and triggers the release of apoptogenic factors, thereby inducing cell death. (nih.gov)
  • 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)
  • 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)
  • 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)
  • 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)
  • p15 BID translocates to mitochondria as an integral membrane protein. (bosterbio.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)
  • 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)
  • 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)
  • Paschen S, Neupert W. Protein import into mitochondria. (labome.org)
  • Degrandi D, Hoffmann R, Beuter Gunia C, Pfeffer K. The proinflammatory cytokine-induced IRG1 protein associates with mitochondria. (labome.org)
  • The intrinsic apoptosis pathway, which involves conserved signaling proteins, is physically associated with mitochondria, and in vertebrates is sensitive to mitochondrial oxidative stress. (creative-diagnostics.com)
  • The anti-apoptotic proteins Bcl-2 and Bcl-XL inhibit cytochrome c release, whereas Bax, Bak, and Bid, all pro-apoptotic proteins, promote its release from mitochondria. (creative-diagnostics.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)
  • 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)
  • 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)
  • 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 contrast, the caspase-resistant mutant Bid D60E and a BH3 defective mutant Bid G94E failed to restore TRAIL-induced apoptosis. (elsevier.com)
  • 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)
  • Concomitantly, emergence of caspase-like enzymatic activity occurs suggesting a role for caspases in the cell death process. (labome.org)
  • The intrinsic apoptosis pathway induces apoptosis by directly activating caspase-3 or by cleaving bid (BH3 interacting domain death agonist), resulting in mitochondrial dysfunction and subsequent release of cytochrome c and activation of caspases-9 and caspases-3. (creative-diagnostics.com)
  • Caspase-3 promotes the typical apoptosis features, including DNA fragmentation and cell death in several tissues. (creative-diagnostics.com)
  • once it has occurred, mitochondrial permeabilization leads to the formation of an apoptosome, which facilitates caspase activation and subsequently triggers the other hallmarks of apoptotic cell death. (creative-diagnostics.com)
  • 9F7-F11 favored the extrinsic apoptosis pathway by inducing TRAIL-R2/DR5 upregulation and TRAIL expression that promoted the formation of death-inducing signaling complex (DISC), leading to caspase-8-mediated apoptosis. (biomedcentral.com)
  • Incubation with 9F7-F11 also induced BID cleavage, BAX upregulation and BIM expression, which initiated the caspase-9/3-mediated mitochondrial death pathway. (biomedcentral.com)
  • This enables recruitment of pro-caspase-8, the inactive form of initiator caspase-8, and formation of the death-inducing signaling complex (DISC). (bioradiations.com)
  • When choosing an apoptosis assay, think about what question you would like to ask - caspase activity assays are excellent indicators of apoptosis initiation whereas DNA fragmentation assays can be used to identify cells in the late stages of apoptosis, when they are irreversibly committed to programmed cell death. (bioradiations.com)
  • The extrinsic pathway activates caspases via cell-surface death receptors, which respond to cognate death ligands expressed on immune-effector cells. (jci.org)
  • 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)
  • Binding of death receptors (Fas, TNF-R, TRAIL-R) to their ligands (Fas-L, TNF, TRAIL) initiates the extrinsic apoptotic pathway. (nih.gov)
  • 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)
  • 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 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 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 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)
  • The extrinsic pathway is triggered by the binding of ligands to death receptors. (bioradiations.com)
  • Upon ligand binding, death receptors oligomerize and recruit adaptor proteins such as FADD. (bioradiations.com)
  • Peroxisomal matrix protein import is mediated by dynamic import receptors, which cycle between the peroxisomal membrane and the cytosol. (bioscirep.org)
  • Peroxisomal matrix proteins are without exception nuclear encoded, synthesized on free ribosomes and subsequently recognized in the cytosol by specific soluble receptors [ 6 , 7 ]. (bioscirep.org)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Together, these results define calpain I-dependent AIF release as a novel signaling pathway that mediates neuronal cell death after cerebral ischemia. (labome.org)
  • The pathway is influenced by members of the Bcl family bound to the mitochondrial membrane, including Bax and Bcl-2 gene, which act as pro- or anti-apoptotic regulatory proteins, respectively. (creative-diagnostics.com)
  • The B-cell lymphoma 2 (Bcl-2) protein family tightly controls activation of the intrinsic pathway. (creative-diagnostics.com)
  • Most chemotherapeutic and targeted cancer therapies kill tumor cells through the generation of pro-death signaling that initiates the intrinsic apoptotic pathway of programmed cell death. (creative-diagnostics.com)
  • The intrinsic pathway (Figure 1) is initiated by Bcl-2 homology proteins. (bioradiations.com)
  • In the classic apoptosis pathway the Bcl-2 proteins Bax and Bak are activated in response to internal stimuli such as DNA damage or oxidative stress. (bioradiations.com)
  • Two distinct yet interconnected signaling pathways control apoptosis by activating a core intracellular machinery of death proteases called caspases. (jci.org)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Activation of this executioner enzyme is irreversible, and results in the cleavage of numerous structural and functional proteins (e.g. (psu.edu)
  • This allows the adaptor molecule ''Fas-associated death domain'' (FADD) to bind the death domain of Fas through its own death domain. (wikidoc.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)
  • 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)
  • Bid/Bik does not interact with the VDAC, but probably has the ability to open an unidentified channel(s) that is involved in cytochrome c release. (nih.gov)
  • 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)
  • The anti-HER3 antibody pro-apoptotic effect occurred concomitantly with downregulation of the pro-survival proteins c-IAP2 and XIAP. (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)
  • Conclusions: Pro-apoptotic proteins involved in both the intrinsic and extrinsic apoptotic pathways were increased significantly by TEGDMA. (umich.edu)
  • Modulation of various cell death pathways by curcumin. (nih.gov)
  • 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)
  • 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)
  • Cellular FLICE-like inhibitory protein (c-FLIP) is a key regulator of apoptotic pathways. (biomedcentral.com)
  • Crosstalk between the intrinsic and extrinsic pathways is mediated via BH-3 interacting domain death agonist (Bid). (bioradiations.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)
  • The C-terminal portion of the protein, known as canstatin, is an inhibitor of angiogenesis and tumor growth. (cancerindex.org)
  • Smac/DIABLO indirectly promotes apoptosis by blocking the effects of a group of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). (creative-diagnostics.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)
  • 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)
  • These two proteins subsequently interact with Bid and are inserted into the outer mitochondrial membrane. (bioradiations.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)
  • 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)
  • 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)
  • 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)
  • The p53 protein is employed as a transcriptional activator of p53-regulated genes. (genome.jp)
  • It is found in follicular lymphoma and first identified as one of the genes involved in the cell death by either activating pro-apoptotic or inhibiting anti-apoptotic apoptosis. (creative-diagnostics.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)
  • Protein microarray-based analyses of the intracellular signaling cascades showed alterations in RTK-AKT/STAT/MAPK signaling cascades, which was subsequently confirmed by Western blotting. (aacrjournals.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)
  • The Bcl-2 family proteins regulate the cellular response to apoptotic stimuli ( 1 , 2 ). (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)
  • Three major clusters of interacting proteins emerged: (a) signaling, (b) DNA repair, and (c) oxidative phosphorylation. (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)
  • 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)
  • FHL2 is a multifunctional adaptor protein with fine-tuning adjustment properties. (readbyqxmd.com)
  • 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)
  • My team developed a recombinant soluble version of the human ligand comprising the extracellular domain of the endogenous protein and possessing a homotrimeric structure. (jci.org)
  • Cell signaling == Fas forms the [[death-inducing signaling complex]] (DISC) upon ligand binding. (wikidoc.org)
  • We conclude that Ynr074cp is a cell death effector in yeast and rename it AIF-1 (Aif1p, gene AIF1). (labome.org)
  • Within minutes following the incidence of an ischemic stroke, necrotic cell death is initiated in the core region of the infarct. (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)
  • 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)
  • 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)
  • Dendra2 is an ideal tool for real-time tracking protein dynamics (movement, degradation, etc.) and monitoring selective cell fate. (clontech.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)
  • 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)
  • Apoptosis is known to play a role in cell death in transient retinal ischemia. (arvojournals.org)
  • 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)
  • 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)
  • 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 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)
  • This trimerization usually leads to apoptosis, or cell death. (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)
  • The anti-apoptotic proteins bind to and inactivate the pro-apoptotic proteins in a healthy cell that does not need to die. (scientificamerican.com)
  • 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)
  • Cell death in the third millennium. (abnova.com)
  • Lockshin RA, Osborne B, Zakeri Z.Cell Death Differ. (abnova.com)
  • Since TRAIL provoked cell death in ESFT ex vivo, this cytokine may be a promising drug for the treatment of ESFT in vivo. (labome.org)
  • Apoptosis is a cell death type that is essential during embryonic development and for homeostasis maintenance. (biomedcentral.com)
  • Apoptosis, or programmed cell death, is a highly regulated way for an organism to selectively eliminate cells. (bioradiations.com)
  • Apoptosis is distinct from unprogrammed cell death/necrosis. (bioradiations.com)
  • However, as we have learned more about apoptosis and necrosis and have identified new mechanisms of cell death such as necroptosis, the lines between apoptosis and necrosis have become more blurred. (bioradiations.com)
  • Description Aplha, transcription related growth factors and stimulating factors or repressing nuclear factors are complex subunits of proteins involved in cell differentiation. (gentaur.com)
  • Intrinsic apoptosis involves BH3-only protein activation of Bax/Bak-mediated mitochondrial outer membrane permeabilization (MOMP). (elsevier.com)
  • Most of these proteins contain a C-terminal putative transmembrane (TM) fragment and a pair of hydrophobic alpha helices (alpha5-alpha6) similar to the membrane insertion fragments of the ion-channel domain of diphtheria toxin and colicins. (jove.com)
  • The functionality of these organelles is governed by dynamically operating import machineries for peroxisomal membrane and matrix proteins [ 1 , 5 ]. (bioscirep.org)
  • We show that the nonstructural HCV viral protein NS5A is sufficient to activate a calpain cysteine protease, leading to degradation of Bid. (cnrs.fr)
  • 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)
  • Moreover we showed that ubiquitination and proteasomal degradation of the anti-apoptotic protein c-FLIP was mediated by USP8-regulated ITCH recruitment. (biomedcentral.com)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Here, we describe a strongly pro-apoptotic BH3-only protein, designated Bbc3, whose expression increases in response to diverse apoptotic stimuli. (pnas.org)
  • 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)
  • Expression changes of cellular proteins were determined by western blot analysis. (biomedcentral.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)
  • 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)
  • and stimulation of key transcription factors such as cAMP-response element binding protein (CREB) and trophic factors such as brain-derived neurotrophic factor (BDNF) ( Hyman, 2006 ). (frontiersin.org)
  • The mature proteins then participate in transcription and replication of the RNA genome and assembly and release of the virus. (asm.org)