Protein factors released from one species of YEAST that are selectively toxic to another species of yeast.
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.
Toxic compounds produced by FUNGI.
Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.
The species Orcinus orca, in the family Delphinidae, characterized by its black and white coloration, and huge triangular dorsal fin. It is the largest member of the DOLPHINS and derives its name from the fact that it is a fearsome predator.
Cytolytic lymphocytes with the unique capacity of killing natural killer (NK)-resistant fresh tumor cells. They are INTERLEUKIN-2-activated NK cells that have no MAJOR HISTOCOMPATIBILITY COMPLEX restriction or need for antigen stimulation. LAK cells are used for ADOPTIVE IMMUNOTHERAPY in cancer patients.
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
A specialized subset of T-LYMPHOCYTES that exhibit features of INNATE IMMUNITY similar to that of NATURAL KILLER CELLS. They are reactive to glycolipids presented in the context of the major histocompatibility complex (MHC) class I-like molecule, CD1D ANTIGEN.
Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.
Agents inhibiting the effect of narcotics on the central nervous system.
Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood.
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
Receptors that are specifically found on the surface of NATURAL KILLER CELLS. They play an important role in regulating the cellular component of INNATE IMMUNITY.

Expression of apoptosis regulatory proteins of the Bcl-2 family and p53 in primary resected non-small-cell lung cancer. (1/716)

Proteins of the Bcl-2 family as well as p53 are important regulators of apoptosis. Alterations in the expression of these proteins can contribute to the formation of cancer, as well as influence tumour response to chemo- and radiotherapy. We used antibodies specific for the human Bcl-2, Mcl-1, Bax, Bak and p53 proteins to examine the expression of these apoptosis-regulating genes in 49 archival specimens of patients with radically resected non-small-cell lung cancer (NSCLC). Tumour cells containing immunostaining for the antiapoptotic proteins Bcl-2 and Mcl-1 were present in 31% and 58% of the cases evaluated, respectively, whereas immunopositivity for the proapoptotic proteins Bax and Bak was found in 47% and 58% of the samples. p53 immunopositivity was detected in 61% of the samples. The expression of Bcl-2 and p53 and the expression of Mcl-1 and Bax showed a positive association (P = 0.02 and P = 0.06 respectively), whereas the expression of Bax was inversely related to p53 (P = 0.008). The expression of Bcl-2 had a negative influence on relapse-free survival in this population of primary resected NSCLC patients (P = 0.02). The expression of p53 and Bcl-2 was significantly associated with metastasis-free survival (P < 0.01). Only patients with p53-positive tumours developed metastases during the follow-up period. Our results establish the frequent expression of the Bcl-2 family proteins Bcl-2, Mcl-1, Bax and Bak in NSCLC. It can be expected that Bcl-2 family members have no straightforward impact on clinical outcome in this disease because their interactions in the regulation of apoptosis are complex.  (+info)

Cell damage-induced conformational changes of the pro-apoptotic protein Bak in vivo precede the onset of apoptosis. (2/716)

Investigation of events committing cells to death revealed that a concealed NH2-terminal epitope of the pro-apoptotic protein Bak became exposed in vivo before apoptosis. This occurred after treatment of human Jurkat or CEM-C7A T-lymphoma cells with the mechanistically disparate agents staurosporine, etoposide or dexamethasone. The rapid, up to 10-fold increase in Bak-associated immunofluorescence was measured with epitope-specific monoclonal antibodies using flow cytometry and microscopy. In contrast, using a polyclonal antibody to Bak, immunofluorescence was detected both before and after treatment. There were no differences in Bak protein content nor in subcellular location before or after treatment. Immunofluorescence showed Bcl-xL and Bak were largely associated with mitochondria and in untreated cells they coimmunoprecipitated in the presence of nonioinic detergent. This association was significantly decreased after cell perturbation suggesting that Bcl-xL dissociation from Bak occurred on exposure of Bak's NH2 terminus. Multiple forms of Bak protein were observed by two dimensional electrophoresis but these were unchanged by inducers of apoptosis. This indicated that integration of cellular damage signals did not take place directly on the Bak protein. Release of proteins, including Bcl-xL, from Bak is suggested to be an important event in commitment to death.  (+info)

Developmental expression patterns of Bcl-2, Bcl-x, Bax, and Bak in teeth. (3/716)

The ontogenic profile of expression of four members of the Bcl-2 family (Bcl-2, Bcl-x, Bax and Bak) was examined in the mouse by immunohistochemistry using paraffin sections. All four members were expressed in changing patterns during critical stages of tooth morphogenesis. Expression was detected in epithelial cell populations including the dental lamina, internal dental epithelium (IDE; differentiating ameloblasts), stratum intermedium and stellate reticulum cells, as well as in the condensed dental mesenchyme. The temporo-spatial localization of the various members of the Bcl-2 family in dental epithelium and mesenchyme showed striking overlapping areas but often their expression patterns differed. In general, contemporaneous co-expression of the Bcl-2 and Bax proteins, and of the Bcl-x and Bak proteins was noted in various types of cells during the developmental process, with the intensity of Bcl-2>Bax and of Bak>Bcl-x. Expression was pronounced at sites where interaction between surface ectoderm and induced mesenchyme takes place, and at the enamel knot, which is regarded as organization/regulating center for tooth development. Around birth, after the structural maturation was accomplished, the expression was down-regulated. The absence of elevated expression of each of these four members of the Bcl-2 family after birth in the teeth suggests that these proteins are relevant during the accomplishment of the basic architecture but not once the structure of the tooth is established.  (+info)

Bak BH3 peptides antagonize Bcl-xL function and induce apoptosis through cytochrome c-independent activation of caspases. (4/716)

The Bcl-2 homology 3 (BH3) domain is crucial for the death-inducing and dimerization properties of pro-apoptotic members of the Bcl-2 protein family, including Bak, Bax, and Bad. Here we report that synthetic peptides corresponding to the BH3 domain of Bak bind to Bcl-xL, antagonize its anti-apoptotic function, and rapidly induce apoptosis when delivered into intact cells via fusion to the Antennapedia homeoprotein internalization domain. Treatment of HeLa cells with the Antennapedia-BH3 fusion peptide resulted in peptide internalization and induction of apoptosis within 2-3 h, as indicated by caspase activation and subsequent poly(ADP-ribose) polymerase cleavage, as well as morphological characteristics of apoptosis. A point mutation within the BH3 peptide that blocks its ability to bind to Bcl-xL abolished its apoptotic activity, suggesting that interaction of the BH3 peptide with Bcl-2-related death suppressors, such as Bcl-xL, may be critical for its activity in cells. While overexpression of Bcl-xL can block BH3-induced apoptosis, treatment with BH3 peptides resensitized Bcl-xL-expressing cells to Fas-mediated apoptosis. BH3-induced apoptosis was blocked by caspase inhibitors, demonstrating a dependence on caspase activation, but was not accompanied by a dramatic early loss of mitochondrial membrane potential or detectable translocation of cytochrome c from mitochondria to cytosol. These findings demonstrate that the BH3 domain itself is capable of inducing apoptosis in whole cells, possibly by antagonizing the function of Bcl-2-related death suppressors.  (+info)

Epstein-Barr virus encodes a novel homolog of the bcl-2 oncogene that inhibits apoptosis and associates with Bax and Bak. (5/716)

The sequenced gammaherpesviruses each contain a single viral bcl-2 homolog (v-bcl-2) which may encode a protein that functions in preventing the apoptotic death of virus-infected cells. Epstein-Barr virus (EBV), a gammaherpesvirus associated with several lymphoid and epithelial malignancies, encodes the v-Bcl-2 homolog BHRF1. In this report the previously uncharacterized BALF1 open reading frame in EBV is identified as having significant sequence similarity to other v-bcl-2 homologs and cellular bcl-2. Transfection of cells with a BALF1 cDNA conferred apoptosis resistance. Furthermore, a recombinant green fluorescent protein-BALF1 fusion protein suppressed apoptosis and associated with Bax and Bak. These results indicate that EBV encodes a second functional v-bcl-2.  (+info)

Developmental regulation of Bcl-2 family protein expression in the involuting mammary gland. (6/716)

Epithelial cells within the mammary gland undergo developmental programmes of proliferation and apoptosis during the pregnancy cycle. After weaning, secretory epithelial cells are removed by apoptosis. To determine whether members of the Bcl-2 gene family could be involved in regulating this process, we have examined whether changes in their expression occur during this developmental apoptotic program in vivo. Bax and Bcl-x were evenly expressed throughout development. However, expression of Bak and Bad was increased during late pregnancy and lactation, and the proteins were present during the time of maximal apoptotic involution. Thereafter, their levels declined. In contrast, Bcl-w was expressed in pregnancy and lactation but was downregulated at the onset of apoptosis. Bcl-2 was not detected in lactating or early involuting mammary gland. Thus, the pro-apoptotic proteins Bax, Bak and Bad, as well as the death-suppressors Bcl-x, Bcl-2 and Bcl-w, are synthesised in mouse mammary gland, and dynamic changes in the expression profiles of these proteins occurs during development. To determine if changes in Bak and Bcl-w expression could regulate mammary apoptosis, their effect on cultured mouse mammary epithelial cells was examined in transient transfection assays. Enforced expression of Bak induced rapid mammary apoptosis, which could be suppressed by coexpression of Bcl-w. In extracts of mammary tissue in vivo, Bak heterodimerized with Bcl-x whereas Bax associated with Bcl-w, but Bak/Bcl-w heterodimers were not detected. Thus, Bak and Bcl-w may regulate cell death through independent pathways. These results support a model in which mammary epithelial cells are primed for apoptosis during the transition from pregnancy to lactation by de novo expression of the death effectors Bak and Bad. It is suggested that these proteins are prevented from triggering apoptosis by anti-apoptotic Bcl-2 family proteins until involution, when the levels of Bcl-w decline. Our study provides evidence that regulated changes in the expression of cell death genes may contribute to the developmental control of mammary apoptosis.  (+info)

Tumor necrosis factor-alpha and lipopolysaccharide induce apoptotic cell death in bovine glomerular endothelial cells. (7/716)

BACKGROUND: The glomerular endothelial cell is a specialized microvascular cell type involved in the regulation of glomerular ultrafiltration. During gram-negative sepsis, glomerulonephritis, and acute renal failure, bacterial lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) may cause severe cell damage. Our aim was to study and compare the direct effects of TNF-alpha and LPS on the induction of apoptosis in bovine glomerular endothelial cells. METHODS: Primary bovine glomerular endothelial cells were stimulated with TNF-alpha or LPS, and apoptotic cell death was investigated by DNA fragmentation analysis, morphological studies, measurement of cytochrome c efflux and mitochondrial permeability transition, Bak, Bad, Bax, Bcl-2, Bcl-xL protein expression, and caspase-3-like protease activity. RESULTS: TNF-alpha, as well as LPS, elicited apoptotic cell death both time and concentration dependently. Along with DNA ladder formation, we detected the formation of 50 kbp high molecular weight DNA fragments, nuclear condensation, and mitochondrial permeability transition. Concerning all parameters, LPS signaling proved to be more rapid than TNF-alpha. Mechanistically, TNF-alpha-induced cell death was preceded by an efflux of mitochondrial cytochrome c into the cytosol and, subsequently, by a marked increase in the proapoptotic protein Bak and a decrease in the anti-apoptotic Bcl-xL protein content. Comparable but more pronounced effects were seen with LPS. Later, caspase-3-like protease activity was first detectable after 10 hours and was continuously increased up to 24 hours in both TNF-alpha- and LPS-stimulated cells. Correspondingly, we detected an extended cleavage of the nuclear enzyme poly(ADP-ribose) polymerase. Caspase inhibitors Z-Asp-CH2-DCB and Z-VAD-fmk blocked both TNF-alpha- and LPS-induced apoptosis in a comparable manner. Only Z-Asp-CH2-DCB was able to block apoptotic cell death completely. CONCLUSION: Both bacterial LPS and TNF-alpha potently induced apoptotic cell death in glomerular endothelial cells. Direct endotoxin-induced apoptosis may therefore be relevant in the progression of acute renal failure, which is a frequent complication of gram-negative sepsis.  (+info)

Human right and left colon differ in epithelial cell apoptosis and in expression of Bak, a pro-apoptotic Bcl-2 homologue. (8/716)

BACKGROUND: Propensity to colonic neoplasia differs between the right and left colon. AIMS: To examine whether this difference may be related to regional differences in epithelial apoptosis, in expression of a proapoptotic regulatory protein, Bak, and in proliferation. PATIENTS: Individuals with no history of colorectal neoplasia. METHODS: Archival blocks of colorectal tissues were immunostained for proliferating cells (antibody to Ki-67 antigen), and Bak expression (polyclonal antiserum). Cells containing DNA strand breaks, a marker of apoptosis, were identified by terminal deoxyuridine nucleotidyl nick end labelling (TUNEL). RESULTS: There were fewer TUNEL positive epithelial cells in the right colon (mean 1.2 (SE 0.1)% of all epithelial cells) than the left colon (2.2 (0.1)%, p<0.0001) or rectum (2.2 (0.3)%, p<0.05). Bak expression was less common in the right colon (mean 46 (2.3)% of epithelial cells immunoreactive) than the left colon (66 (2.7)%, p<0.0001), or rectum (67 (2.3)%, p<0.001). Bak expression and TUNEL positivity were highly positively correlated (p<0.0001). In contrast to apoptosis, mean whole crypt proliferation labelling index was similar throughout the colorectum (right colon: 15.6 (3.2)%; left colon: 13. 5 (1.2)%; rectum: 13.3 (2.3)%). CONCLUSION: The percentage of proliferating colonic epithelial cells is constant throughout the colon, but fewer epithelial cells undergo Bak mediated apoptosis in the right than in the left colon or rectum. This suggests that colonocytes may be lost by methods other than apoptosis in the right colon.  (+info)

Critical issues in apoptosis include the importance of caspases versus organelle dysfunction, dominance of anti- versus proapoptotic BCL-2 members, and whether commitment occurs upstream or downstream of mitochondria. Here, we show cells deficient for the downstream effectors Apaf-1, Caspase-9, or C …
Functional interaction of Bcl-2/Bcl-xL and Bax/Bak, but not Bid/Bik, with the VDAC. Bax/Bak directly opens the VDAC to induce cytochrome c release, while Bcl-2/
Apoptosis mediated by the proapoptotic BCL-2 family members BCL-2-associated X-protein (BAX) and BCL-2 antagonist/killer (BAK) is part of the antiviral response at the cellular level to limit virus replication. Viruses, in turn, have evolved to encode antiapoptotic BCL-2 homologs (v-BCL-2s) to preve …
Mouse anti Human BAK antibody recognizes the Bcl-2 homologous antagonist/killer, also known as BAK, BCL2-like 7 protein, apoptosis regulat
Bak小鼠单克隆抗体[AT8B4](ab104124)可与小鼠, 人样本反应并经WB, ELISA, ICC/IF实验严格验证。中国75%以上现货,所有产品提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
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Nyrene er et par små, bønneformede organer lokalisert bak mot ryggen i bukhulen og beskyttet av de nederste ribbena. Nyrenes funksjon er å filtrere av...
Ataxia telangiectasia (AT) is an autosomal recessive multisystem disorder characterized by variable immunodeficiency, progressive neurodegeneration, occulocutaneous telangiectasia, and an increased susceptibility to malignancies. This study was designed to study the role of proapoptotic BAK, BAX, and NBK/BIK genes in a group of patients with AT to elucidate the possible role of these genes in progression of malignancies in this disease. Fifty Iranian patients with AT were investigated in this study. The entire coding regions of the BAK gene (exons 2-6), NBK/BIK gene (exons 2-5), and BAX gene (exons 1-7) were amplified using polymerase chain reaction (PCR). The PCR products were separated by 2% agarose gel electrophoresis, and all positive samples were verified by direct sequencing of PCR products using the same primers used for PCR amplification, BigDye chemistry, and Avent 3100 Genetic Analyzer following the manufacturers instructions (Applied Biosystems). Eight of fifty Iranian AT patients (16%)
Although GT has long been proposed to constitute a virulence factor in IA (Eichner and Mullbacher, 1984; Mullbacher and Eichner, 1984), most probably by suppressing immune responses via induction of mammalian cell apoptosis (Waring et al., 1988b; Sutton et al., 1994), the molecular mechanisms underlying the putative in vitro and in vivo processes have not been elucidated. Here, we present evidence that Bak, but not Bax, is a key host factor in GT-mediated cell death in vitro. We used MEFs and FDMs deficient in the Bcl-2 family members Bak and/or Bax or their activator Bid (Wei et al., 2000) and isolated mitochondria from these cells to show that GT-mediated activation of Bak occurs independently of Bid or other cytosolic factors. Once activated, Bak triggers the generation of ROS, which is crucial for effective mitochondrial membrane pore formation, including the release of cytochrome c and AIF, and ultimate cell death. The additional finding that the virulence of GT-producing A. fumigatus was ...
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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 ...
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 ...
Supplementary Materialsoncotarget-10-6219-s001. domains. BH3-only proteins can straight bind and activate BAX/BAK or can put their amphipathic BH3 -helix right into a groove on anti-apoptotic proteins target(s) leading to release and following indirect BAX/BAK activation [1]. Cancers cells have always been recognized to evade cell loss of life through overexpression of anti-apoptotic BCL-2 associates or through down-regulation of BH3-just proteins [1]. To get over these hurdles theres a great pharmacologic crusade to build up agents that straight engage BCL-2 family members proteins to induce loss of life whatever the cells origins or hereditary perturbations [2]. Despite early guarantee, many BH3-mimetics, never have translated towards the medical clinic or have already been which can function successfully, at least partly, in addition to the BCL-2 network [3C5]. Functional redundancy inside the BCL-2 family members makes it complicated to tailor effective healing strategies without incurring ...
Another mechanism by which the UPR could impact on cell death is the IRE1α pathway. Bak/Bax were suggested to directly interact with IRE1α resulting in activation of JNK (Hetz et al., 2006). However, neither the knockout of IRE1α, JNK nor other components of this pathway or JNK inhibition conferred protection from ER stress. Our observation that death of ire1α-/- cells was caspase dependent, whereas it was caspase independent in bak/bax-/- cells, rather suggests that Bak/Bax and IRE1α are acting on separate pathways.. In WT and Bak/Bax-deficient MEFs ER stress rapidly induced autophagic alterations. This indicates that autophagic alterations per se are independent of proapoptotic Bcl-2 proteins. Autophagy has been implied as a death mechanism substituting for deficient apoptosis under certain conditions (Levine and Yuan, 2005; Maiuri et al., 2007). Interestingly, autophagy was more pronounced in bak/bax-/- than in WT cells, as judged by an increased occurrence of autophagic vacuoles and ...
A critical hallmark of tumor cell success is evasion of apoptosis. Mcl-1 or Bcl-2. Finally BH3-M6 sensitizes cells to apoptosis induced from the proteasome inhibitor CEP-1612. Bim Poor Bik Bmf Bet Noxa and Puma) (5). Multi-domain pro-apoptotic protein Bax and Bak are definitely necessary for apoptosis (2). In response to mobile tension they induce the discharge from mitochondria of apoptogenic elements such as for example cytochrome as well as the initiation of intrinsic apoptosis. Nevertheless triggered Bax and Bak still could be kept in balance by binding to anti-apoptotic Bcl-2 protein (8 -10). X-ray diffraction and nuclear magnetic resonance (NMR) research have shown how the amphipathic α-helices of pro-apoptotic protein such as for example Bak or Poor BH3 domains match a hydrophobic pocket shaped from the BH1 BH2 and BH3 domains of Bcl-2 Bcl-XL and Mcl-1 (11). When BH3-just protein bind to anti-apoptotic Bcl-2 protein multi-domain protein Bak or Bax become absolve to induce apoptosis (12). ...
Failure of the pancreatic β-cells to compensate for high insulin needs is central to the pathogenesis of T2D, and several studies have reported a significant decrease in β-cell mass in T2D (2,26). Chronic exposure to FFAs causes loss of functional β-cell mass (34,35) and may contribute to T2D. Saturated lipids are harmful to β-cells, and pronounced ER stress signaling (especially in the PERK pathway) has been proposed to mediate lipotoxic apoptosis (7-10,15). Execution of FFA-induced apoptosis occurs through the mitochondrial pathway, as indicated by cytochrome c release from the mitochondria after palmitate treatment (13,36,37), but it remained to be clarified how palmitate-induced ER stress crosstalks with the mitochondria to culminate in β-cell death. We have now answered this question, showing that palmitate transcriptionally induces the BH3-only proteins DP5 and PUMA through PERK-dependent ATF3 expression (Fig. 6G).. In the hierarchical model for Bax/Bak activation, the BH3-only ...
Immunocytochemical Expression of BAX and BAK Proteins in Cervical Smears of Women Positive for HPV Types: A Study of 120 Cases
The human lymphocyte toxins granzyme B (hGrzB) and perforin cooperatively induce apoptosis of virus-infected or transformed cells: perforin pores enable entry of the serine protease hGrzB into the cytosol, where it processes Bid to selectively activate the intrinsic apoptosis pathway. Truncated Bid (tBid) induces Bax/Bak-dependent mitochondrial outer membrane permeability and the release of cytochrome c and Smac/Diablo. To identify cellular proteins that regulate perforin/hGrzB-mediated Bid cleavage and subsequent apoptosis, we performed a gene-knockdown (KD) screen using a lentiviral pool of short hairpin RNAs embedded within a miR30 backbone (shRNAmiR ...
Induction of the generation of endoplasmic reticulum (ER) calcium (Ca(++))-mediated reactive oxygen species (ROS) by gallic acid (GA) has been implicated in the mitochondrial apoptotic death of human oral cancer (OC) cells, but the molecular mechanism by which GA causes ER Ca(++) release of OC cells to undergo cell death remains unclear. Here, we report that GA-induced phosphorylation of B-cell lymphoma 2 (BCL-2)-interacting killer (BIK) (threonine (Thr) 33/Serine (Ser) 35) and p53 (Ser 15 and Ser 392), Bcl-2-associated x protein (BAX)/BCL-2 antagonist killer 1 (BAK) oligomerization on the ER and mitochondria, rising of cytosolic Ca(+)(+) and ROS, cytochrome c (Cyt c) release from the mitochondria, Ψm loss, and apoptosis were suppressed in cells co-treated with a specific inhibitor of casein kinase II (CK II) (4,5,6,7-tetrabromobenzotriazole ...
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Many proteins are involved. Bcl-2 is an anti-apoptotic protein, while BAD, BAX and BAK are pro-apoptotic. Bcl-2 contains 5 segments. BH1, BH2, BH3, BH4 and a TM segment. The BH4 segment is the segment that makes Bcl-2 anti-apoptotic. BAK and BAX contain the same segments except BH4, which make them pro-apoptotic. BAD contains only BH3, and is therefore also pro-apoptotic as it lacks BH4.. The intrinsic pathway is largely dependent on the mitochondria. Certain stimuli such as DNA damage, ER stress, hypoxia or metabolic stress. These stimuli activate BAD. BAD then activates BAX and BAK which form a pore in the outer mitochondrial membrane called MAC. This increases the permeability of the outer mitochondrial membrane, a process called mitochondrial outer membrane permeabilization or MOMP, which allows molecules from inside the mitochondria will migrate out into the cytoplasm. In particular, cytochrome C, DIABLO (or SMAC), AIF and EndoG are released.. DIABLO is a protein that inhibits a protein ...
The purpose of this study was to determine whether recombinant human growth hormone (rhGH) would show any significant effects on the expression of apoptosis regulating proteins in peripheral blood mononuclear cells (PBMCs). Additionally, the potential for post-transcriptional regulation of gene expression by miRNA was assessed in two cellular compartments, the cytosol and the mitochondria. Ten male subjects were subcutaneously injected with either rhGH (1 mg) or saline (0.9%) for seven consecutive days in a double-blinded fashion. Blood sampling was undertaken prior to treatment administration and over a period of three weeks following treatment cessation. Bcl-2 and Bak gene and protein expression levels were measured in PBMCs, while attention was also directed to the expression of miR-181a and miR-125b, known translational inhibitors of Bcl-2 and Bak respectively. Results showed that rhGH significantly decreased Bak protein concentrations compared to placebo samples for up to 8 days post treatment.
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 ...
Looking for BAK? Find out information about BAK. A popular extension for a file that duplicates an original of any type. See backup and file extension Explanation of BAK
The BH4 region is highly conserved in sequence among the three closest homologues in the mammalian Bcl‐2 family, Bcl‐2, Bcl‐xL and Bcl‐w (Figure 1), and we have shown that BH4 of Bcl‐x can substitute for that of Bcl‐2 (Figure 4). The structure of Bcl‐xL indicates that the BH4 region encompasses an amphipathic α‐helical loop on the surface that forms extensive hydrophobic interactions with α2, α5 and α6 (Muchmore et al., 1996). Although the N‐terminal regions of Bax and Bak may also contain an amphipathic helix (Muchmore et al., 1996), sequence homology is minimal (Figure 1) and replacement of the BH4 region of Bcl‐2 with the putative Bax helix inactivated Bcl‐2 (Figure 4).. Since the BH4 region is the only conserved domain that sets these pro‐survival members of the Bcl‐2 family apart from their pro‐apoptosis relatives (Figure 1), we assessed how point mutations introduced into that region of Bcl‐2 affected its survival function. We found that most single amino ...
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Dik PP, Danilova IG, Golubev IS, Kazakov MO, Nadeina KA, Budukva SV, Pereyma VY, Klimov OV, Prosvirin IP, Gerasimov EY, Bok TO, Dobryakova IV, Knyazeva EE, Ivanova II, Noskov ...
BAK is the most prevalent and its cytotoxicity is well-documented. Reports have shown that BAK can accumulate in ocular tissue and can cause different types of cell death with frequent dosing. Its thought that patients at greatest risk for BAK-induced adverse effects are those suffering from dry eyes. Because of the lack of natural tears in these patients, the BAK in each eye drop is not as diluted as it would be in a patient with normal tear formation. This may damage the corneal epithelium (top layer of the eye) contributing to ocular surface disease. (Using more than 4 - 6 drops per day increases the likelihood of BAK-induced adverse effects ...
The Bcl-2 family of proteins regulates mitochondrial outer membrane permeabilization (MOMP) - considered as the point-of-no-return in apoptosis. As the gatekeeper for survival or death of cells, this network is tightly regulated by interactions of its members with opposing functions. The embedded together model remains as one of the most accepted models to describe the interactions between family members. This model highlights the role of the mitochondrial membrane to augment these interactions. And while this model has been repeatedly exemplified in vitro, the e↵ect of membranes on Bcl-2 protein interactions has not yet been fully explored in living cells. On the other hand, the Bcl-2 proteins could also a↵ect the physical properties of the membrane. Bax and Bak are the main e↵ectors of apoptosis, believed to form pores on the mitochondrial outer membrane. However, no one has seen an apoptotic pore. Aside from its permeabilizing activity, the e↵ect of Bcl-2 proteins on the physical ...
Colorectal cancer (CRC) is the third leading cause of cancer-related death in the United States. During the tumorigenesis and metastasis of CRC, cells encounter numerous cellular and molecular events. ATF3, a member of the ATF/CREB transcription factor family, plays an important role on regulation of apoptosis and is regarded as a potential molecular target for chemoprevention and chemotherapy of colon cancer. The current study was performed to investigate cellular and molecular mechanisms by which ATF3 affects colon cancer-related phenotypes including apoptosis and metastasis. Here, we demonstrated that knockdown of ATF3 using small interfering RNA (siRNA) promotes the expression of anti-apoptotic protein, B-cell lymphoma 2 (Bcl-2), in colon cancer cells, while overexpression of ATF3 resulted in a dramatic decrease in Bcl-2 protein. Gain of function of ATF3 in colon cancer cell line HCT116 led to an increase of pro-apoptotic protein Bcl-2 homologous antagonist killer (Bak), followed by the ...
Background Obatoclax is a clinical stage medication candidate that is proposed to focus on and inhibit prosurvival people from the Bcl-2 family members, and thereby donate to cancers cell lethality. totally partitioned into liposomal lipid but also quickly exchanged between liposome contaminants. In this technique, obatoclax was discovered to be always a immediate and powerful antagonist of liposome-bound Mcl-1 however, not of liposome-bound Bcl-XL, and didnt directly impact Bak. A 2.5 molar more than obatoclax in accordance with Mcl-1 overcame Mcl-1-mediated inhibition of tBid-Bak activation. Very similar results had been discovered for induction of Bak oligomers by Bim. Obatoclax exhibited powerful lethality within a cellmodel reliant on Mcl-1 for viability however, not in cells reliant on Bcl-XL. Molecular modeling predicts which the 3-methoxy moiety of obatoclax penetrates in to the P2 pocket from the BH3 binding site of Mcl-1. A desmethoxy derivative of obatoclax didnt inhibit Mcl-1 in ...
Apoptosis is a genetically programmed process for the elimination of damaged or redundant cells by activation of caspases (aspartate-specific cysteine proteases). The onset of apoptosis is controlled by numerous interrelating processes. The extrinsic pathway involves stimulation of members of the tumor necrosis factor (TNF) receptor subfamily, such as TNFRI, CD95/Fas or TRAILR (death receptors), located at the cell surface, by their specific ligands, such as TNF-alpha, FasL or TRAIL, respectively. The intrinsic pathway is activated mainly by non-receptor stimuli, such as DNA damage, ER stress, metabolic stress, UV radiation or growth-factor deprivation. The central event in the intrinsic pathway is the mitochondrial outer membrane permeabilization (MOMP), which leads to the release of cytochrome c. These two pathways converge at the level of effector caspases, such as caspase-3 and caspase-7. The third major pathway is initiated by the constituents of cytotoxic granules (e.g. Perforin and ...
To our knowledge, maspin is the only serpin that sensitizes apoptosis, whereas all of the other serpins thus far implicated in apoptosis regulation appear to be antiapoptotic (17 , 32 , 33) . Thus, the existing literature offers little insight into the possible molecular mode of maspin action. The goal of the present study was to identify the specific target molecule(s), the modification of which by maspin sensitizes prostate and breast tumor cells toward potential cancer chemotherapeutic agents. By using multiple maspin-transfected cell lines in vitro, we obtained cellular, molecular, and biochemical evidence that supports a key role for Bax in maspin-mediated apoptosis sensitization. Although we may not have exhausted our search because of the ever-growing number of apoptosis regulators, our data seem sufficient to support our new hypothesis that the specific up-regulation of Bax, without changing Bcl-2, Bcl-xl, and Bak expression in maspin-transfected cells, may tip the balance of pro- versus ...
Proapoptotic BCL-2 family BAX and BAK are necessary for the initiation of mitochondrial dysfunction during apoptosis as well as for maintaining the endoplasmic reticulum (ER) Ca2+ stores essential for Ca2+-reliant cell death. didnt make any additive upsurge in [Ca2+]er, in keeping with these protein employed in a linear pathway to regulate ER Ca2+. After achieving [Ca2+]er steady condition, leak was assessed after addition of tBuBHQ towards the perfusate. Knocking down IP3R-1 considerably decreased ER Ca2+ drip in DKO cells for an intermediate level between that of WT and DKO cells transfected with control RNAi (Fig. 4 0.05; Students check). The difference in [Ca2+]er between BCL-2- and IP3R-1 RNAi-transfected DKO cells isnt statistically significant. (launch, or in the ER, where they regulate [Ca2+]er and Ca2+-reliant death indicators (3, 11). How these substances perform such varied functions is usually a critical staying question. Right here we explored the system where ablation of BAX and ...
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... by inhibiting the apoptosis-causing proteins, Bcl-2-associated X protein and Bcl-2 homologous antagonist killer. BCL6: This ... Pharmacological inhibition of BCL-2 is effective in most B cell lymphomas, but often leads to acquired resistance due to the ... Gene and protein markers in the neoplastic cells of DLBCL, NOS that have clinical significance include CD5, MYC, BCL2, BCL6, ... As indicated in the following Treatments and prognoses section, expression of the CD20 and CD30 proteins as well as the CD19, ...
The same design principle has been applied to inhibit protein-protein interactions involved in cancer and can be used for any ... Chemistry portal Biology portal Photochromism Azobenzene Spiropyran Diarylethene Photodynamic therapy Bcl-2 Bak (Bcl-2 ... homologous antagonist killer) Bid (BH3 interacting-domain death agonist) Luis Moroder, G. Andrew Woolley, Rudolf K. Allemann, ... Photoswitchable peptides to inhibit protein-protein interactions in a light-controlled manner have been developed and applied ...
... a protein involved in pro-apoptotic action Biking Across Kansas Basic Aeronautical Knowledge Bäk, a municipality in the ... a DOS-based role-playing video game Bill and keep reciprocal payment in telecommunications systems Bcl-2 homologous antagonist ... killer, ...
Another example of TSAs are abnormal products of mutated oncogenes (e.g. Ras protein) and anti-oncogenes (e.g. p53). Tumor- ... Bcl-2, IAP or XIAP. Production of TGF-β by tumor cells and other cells (such as myeloid-derived suppressor cell) leads to ... TSAs can be products of oncoviruses like E6 and E7 proteins of human papillomavirus, occurring in cervical carcinoma, or EBNA-1 ... Weon JL, Potts PR (December 2015). "The MAGE protein family and cancer". Current Opinion in Cell Biology. 37: 1-8. doi:10.1016/ ...
These pro-apoptotic proteins are in turn activated by BH3-only proteins, and are inhibited by the function of BCL-2 and its ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". The ... The pro-apoptotic proteins in the BCL-2 family, including Bax and Bak, normally act on the mitochondrial membrane to promote ... Tagami S, Eguchi Y, Kinoshita M, Takeda M, Tsujimoto Y (November 2000). "A novel protein, RTN-XS, interacts with both Bcl-XL ...
This protein also interacts with the tumor suppressor P53 after exposure to cell stress. BAK1 is a pro-apoptotic Bcl-2 protein ... "Entrez Gene: BAK1 BCL2-antagonist/killer 1". Westphal D, Kluck RM, Dewson G (February 2014). "Building blocks of the apoptotic ... The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act ... two proteins of the mitochondrial protein sorting and assembly machinery, are essential for Bak activation during TNF alpha ...
... bcl-associated death protein MeSH D12.644.360.075.718.400 - bcl-2-associated x protein MeSH D12.644.360.075.718.750 - bcl-2 ... homologous antagonist-killer protein MeSH D12.644.360.075.718.937 - bcl-x protein MeSH D12.644.360.075.718.968 - bh3 ... x-linked inhibitor of apoptosis protein MeSH D12.644.360.075.718 - proto-oncogene proteins c-bcl-2 MeSH D12.644.360.075.718.100 ... 14-3-3 proteins MeSH D12.644.360.024.318 - proto-oncogene proteins c-crk MeSH D12.644.360.024.326 - proto-oncogene proteins c- ...
In the intrinsic pathway, ROS function to facilitate cytochrome c release by activating pore-stabilizing proteins (Bcl-2 and ... Bcl-xL) as well as inhibiting pore-destabilizing proteins (Bcl-2-associated X protein, Bcl-2 homologous antagonist/killer). The ... causing oxidized protein levels to increase. This led researchers to conclude that oxidation of cellular proteins is ... The altered protein expression in neurons, controlled in part by ROS-dependent demethylation of CpG sites in gene promoters ...
... bcl-associated death protein MeSH D12.776.476.075.718.400 - bcl-2-associated x protein MeSH D12.776.476.075.718.425 - bcl-2 ... homologous antagonist-killer protein MeSH D12.776.476.075.718.875 - bcl-x protein MeSH D12.776.476.075.718.937 - bh3 ... smad1 protein MeSH D12.776.476.024.417.500.200 - smad2 protein MeSH D12.776.476.024.417.500.300 - smad3 protein MeSH D12.776. ... smad proteins, inhibitory MeSH D12.776.476.024.417.249.600 - smad6 protein MeSH D12.776.476.024.417.249.700 - smad7 protein ...
... associated X protein/Bcl‑extra large ratio in A549 cells. These findings suggest that FCP induced G2/M arrest and apoptosis of ... Slee EA, Adrain C and Martin SJ: Serial killers: ordering caspase activation events in apoptosis. Cell Death Differ. 6:1067- ... The protein content was quantified using a Bradford assay (Bio-Rad Laboratories, Inc.). Proteins were separated by 12% sodium ... whereas the expression of the proapoptotic Bax protein was unchanged, and the ratio of Bax/Bcl-xL was dose-dependently ...
... bcl-X protein - metabolism ; Proto-oncogene proteins c-bcl-2 - metabolism ; Blotting, Western. Charakt. formalna: Zagraniczne ... Angielskie s owa kluczowe: Graves' disease - pathology ; Goiter, nodular - pathology ; Proto-oncogene proteins c-bcl-2 - ... Tytu orygina u: Identification of proapoptotic (BAK,BAX) and antiapoptotic (BCL-xL), BCL-2) proteins in thyrocytes from ... Proto-oncogene proteins c-bcl-2 - biosynthesis ; Thyrotropin - blood ; Thyroxine - blood ; Triiodothyronine - blood. Charakt. ...
BH3-only proteins of the Bcl-2 family, Bim and Puma, are required for the initiation of apoptosis by multiple stimuli, ... To confirm that Dex-dependent cell death and E4BP4 and Bim upregulation are dependent on GR, the effects of the GR antagonist ... E4BP4 has been shown to induce differentiation in monocyte-macrophages [50], to drive natural killer cell lineage development [ ... The mouse and human E4BP4 genes are highly homologous, with 79% nucleotide sequence identity in the coding region. The two ...
BCL2 Antagonist/Killer 1) ELISA Kit based in Delhi, India ... Rat BAK1(BCL2 Antagonist/Killer 1) ELISA Kit. *Rat BAX(BCL-2 ... Rat SP-A1(Pulmonary surfactant-associated protein A1) ELISA Kit. *Rat SP-A1(Pulmonary surfactant-associated protein A1) ELISA ... Rat BAK1(BCL2 Antagonist/Killer 1) ELISA Kit Synonyms:BAK, BAK-LIKE, BCL2L7, CDN1, Bcl-2 Homologous Antagonist/Killer. Intended ... Get a price quote for Rat BAK1(BCL2 Antagonist/Killer 1) ELISA Kit ...
... protein flare C SCANS studie C-486 C-ALCL C-ETACs as hallmarks of cancer C-ion RT C-reactive protein C-reactive protein ... BBD-BC BCBM BCC BCCs BCCSS BCG BCG vaccination in childhood BCG-unresponsive non-muscle-invasive bladder cancer BCIN+ BCIS Bcl- ... agonists versus GnRH antagonists CVD risk factors CVD risk factors and colorectal cancer CVEs CVSS-studie CXB CXCL8-CXCR1 2 ... levels cytokine-induced killer cell therapy cytokines cytology testing cytoreductive surgery Cytosponge-trefoil factor 3 D-2- ...
Keywords: فاکتور رشد اندوتلیال عروقی (VEGF); AP-1; activator protein-1; Bax; Bcl-2-associated X protein; Bcl-2; B cell lymphoma ... C/EBP-homologous protein 10; DNA; dezoxiribonucleic acid; FITC; fluorescein isothiocyanate; GAPDH; (Glyceraldehyde 3-phosphate ... Keywords: فاکتور رشد اندوتلیال عروقی (VEGF); AMPK; AMP-activated protein kinase; ARF6; ADP-ribosylation factor 6; AKT; protein ... autophagy protein; BAK; Bcl 2 homologous antagonist/killer; BAX; Bcl-2 associated -X protein; Bcl-2; B- ...
Sperm postacrosomal WW domain-binding protein is not required for mouse egg activation. C/EBP homologous protein deficiency ... Bcl-xL Displays Restricted Distribution during T Cell Developement and Inhibits Multiple Forms of Apoptosis but Not Clonal ... T Cell Receptor Antagonist Peptides Induce Positive Selection. Tissue-specific knockout of the mouse Pig-a gene reveals ... Reversible Defects in Natural Killer and Memory CD8 T Cell Lineages in Interleukin 15-deficient Mice. Differential T Cell ...
... homologous antagonist killer (Bak), BCL-2-associated X protein (Bax), and cytochrome c at both the mRNA and protein levels were ... and MCP-1 protein expression, increase IκB protein expression in HPASMCs. According to what we observed, this study indicated ... and increased cell cycle inhibitor proteins p21. Besides, ASE decreased the total protein level of epidermal growth factor ... At the cellular and molecular levels, we found that 18β-GA could significantly reduce the accumulation of misfolded protein in ...
B cell lymphoma 6 protein (BCL-6), was identified183,184,185. TFH cells represent a specialized subset of CD4+ T cells that ... Self-amplifying mRNA vaccines expressing multiple conserved influenza antigens confer protection against homologous and ... antagonist increased the cytolytic capacity of CD8+ T cells and modestly delayed tumour growth in OVA-expressing lymphoma or ... Tumor associated antigen and interleukin-12 mRNA transfected dendritic cells enhance effector function of natural killer cells ...
Protein metabolism ‎]] #[[Prozone ‎]] #[[Robert W. Holley ‎]] #[[Röntgen equivalent man ‎]] #[[SUMO protein ‎]] #[[ ... Homologous series ‎]] #[[ICD-10 Chapter K ‎]] #[[Cementum ‎]] #[[Chronic stable angina historical perspective ‎]] #[[Cluster of ... Antagonist (muscle) ‎]] #[[Anti-ganglioside antibodies ‎]] #[[Arcuate vein ‎]] #[[Arene substitution patterns ‎]] #[[ATC code H ... Natural Killer T cell ‎]] #[[Dichloromethane ‎]] #[[Extensor hallucis longus muscle ‎]] #[[Exudate ‎]] #[[Failure to thrive ...
Protein fabrication automation. * Protein isoforms encoded by the pX region of human T-cell leukemia/lymphotropic virus type I. ... Frequent detection of bcl-2/JH translocations in human blood and organ samples by a quantitative polymerase chain reaction ... Identification and mapping of type 1 neurofibromatosis (NF1) homologous loci. * Identification of Aedes aegypti and its ... cDNA cloning of an intracellular form of the human interleukin 1 receptor antagonist associated with epithelium. ...
Expression of WAVEs, the WASP (Wiskott-Aldrich syndrome protein) family of verprolin homologous proteins in human wound tissues ... The role of Bik1 (BCL-2 interaction killer) in wound healing [Abstract]. Wound Repair and Regeneration 18(6), pp. A92. (10.1111 ... for resistance and recurrence after conventional chemotherapy and also the recently introduced smoothened antagonists. ... Expression of WAVEs, the WASP (Wiskott-Aldrich syndrome protein) family of verprolin homologous proteins in human wound tissues ...
antagonist blocks histamine-induced proinflammatory cytokine production through inhibition of Ca2+-dependent protein kinase C, ... Regulation of expression of Bcl-3 proto-oncogene by IKK ϵ. *Regulation of I-kappa-B kinase (IKK) Pathway by CARMA 1• Bcl-10• ... IKK-i and TBK-1 are Enzymatically Distinct from the Homologous Enzyme IKK-2 COMPARATIVE ANALYSIS OF RECOMBINANT HUMAN IKK-i, ... Deficient natural killer cell cytotoxicity in patients with IKK-γ/NEMO mutations ...
... promotes cancer metastasis through resistance to anoikis and increased invasiveness Co-targeting of BAX and BCL-XL proteins ... Reparative effects of interleukin-1 receptor antagonist in young and aged/co-morbid rodents after cerebral ischemia Epithelial- ... pylori infection in a pig model is dominated by Th1 and cytotoxic CD8+ T cell responses Epigenetic control of natural killer ... microtissue and its application for adverse drug reaction assay Non-catalytic roles for XPG with BRCA1 and BRCA2 in homologous ...
Many viruses encode proteins that can inhibit apoptosis.[104] Several viruses encode viral homologs of Bcl-2. These homologs ... such as Natural Killer and cytotoxic T cells) that then induce the infected cell to undergo apoptosis.[99] ... The adenovirus E1B-55K protein and the hepatitis B virus HBx protein are examples of viral proteins that can perform such a ... these inhibitory proteins target retinoblastoma tumor-suppressing proteins.[84] These tumor-suppressing proteins regulate the ...
... promotes cancer metastasis through resistance to anoikis and increased invasiveness Co-targeting of BAX and BCL-XL proteins ... Reparative effects of interleukin-1 receptor antagonist in young and aged/co-morbid rodents after cerebral ischemia Epithelial- ... pylori infection in a pig model is dominated by Th1 and cytotoxic CD8+ T cell responses Epigenetic control of natural killer ... microtissue and its application for adverse drug reaction assay Non-catalytic roles for XPG with BRCA1 and BRCA2 in homologous ...
... protein-coding genes corresponding to TFs (from TransmiR), and signaling proteins (from TransmiR). The triangle denotes the ... Guirouilh-Barbat JK, Wilhelm T, Lopez BS: AKT1/BRCA1 in the control of homologous recombination and genetic stability: the ... MicroRNA-125b confers the resistance of breast cancer cells to paclitaxel through suppression of pro-apoptotic Bcl-2 antagonist ... killer 1 (Bak1) expression. J Biol Chem. 2010, 285: 21496-21507. 10.1074/jbc.M109.083337. ...
... bcl-X protein - metabolism. Charakt. formalna: Zagraniczny artyku Charakt. merytoryczna: Praca oryginalna. J zyk publikacji: ... Tytu orygina u: Coexistence of homologous-type cervical carcinosarcoma with endometrioid-type G1 endometrial cancer: a case ... bcl-X protein - metabolism. Charakt. formalna: Zagraniczny artyku Charakt. merytoryczna: Praca oryginalna. J zyk publikacji: ... bcl-X protein - metabolism. Charakt. formalna: Zagraniczny artyku Charakt. merytoryczna: Praca oryginalna. J zyk publikacji: ...
2. However, to our knowledge, mitochondrial double-stranded RNA has not been previously characterized in vivo. Here we describe ... bcl-2 Homologous Antagonist-Killer Protein, bcl-2-Associated X Protein ... 2. However, to our knowledge, mitochondrial double-stranded RNA has not been previously characterized in vivo. Here we describe ...
Direct interaction of the mitochondrial membrane protein carnitine palmitoyltransferase I with Bcl-2. Biochem Biophys Res ... Clinical safety and activity of AG-120, a first-in-class, potent inhibitor of the IDH1 mutant protein, in a phase 1 study of ... Protein synthesis is resistant to rapamycin and constitutes a promising therapeutic target in acute myeloid leukemia. Blood. ... BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells. Cell Stem ...
For example, adenoviruses and some gamma-herpesviruses express homologs of prosurvival Bcl-2 to subvert the host's apoptotic ... Many viruses express antiapoptotic proteins to counter host defense mechanisms that would otherwise trigger the rapid clearance ... These findings expand the family of protein sequences that act like Bcl-2 to block apoptosis and support the conclusion that ... A structural viral mimic of prosurvival Bcl-2: a pivotal role for sequestering proapoptotic Bax and Bak Mol Cell. 2007 Mar 23; ...
For example, adenoviruses and some gamma-herpesviruses express homologs of prosurvival Bcl-2 to subvert the hosts apoptotic ... Many viruses express antiapoptotic proteins to counter host defense mechanisms that would otherwise trigger the rapid clearance ... These findings expand the family of protein sequences that act like Bcl-2 to block apoptosis and support the conclusion that ... A structural viral mimic of prosurvival Bcl-2: a pivotal role for sequestering proapoptotic Bax and Bak Mol Cell. 2007 Mar 23; ...
This protein also interacts with the tumor suppressor P53 after exposure to cell stress. BAK1 is a pro-apoptotic Bcl-2 protein ... "Entrez Gene: BAK1 BCL2-antagonist/killer 1". Westphal D, Kluck RM, Dewson G (February 2014). "Building blocks of the apoptotic ... The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act ... two proteins of the mitochondrial protein sorting and assembly machinery, are essential for Bak activation during TNF alpha ...
Induction of Androgen Receptor-Dependent Apoptosis in Prostate Cancer Cells by the Retinoblastoma Protein. ... bcl-2 Homologous Antagonist-Killer Protein 11% * Mitochondria 11% * Genetic Suppression 10% ... Induction of Androgen Receptor-Dependent Apoptosis in Prostate Cancer Cells by the Retinoblastoma Protein. Together they form ...
... associated X protein/Bcl‑extra large ratio in A549 cells. These findings suggest that FCP induced G2/M arrest and apoptosis of ... Slee EA, Adrain C and Martin SJ: Serial killers: ordering caspase activation events in apoptosis. Cell Death Differ. 6:1067- ... The protein content was quantified using a Bradford assay (Bio-Rad Laboratories, Inc.). Proteins were separated by 12% sodium ... whereas the expression of the proapoptotic Bax protein was unchanged, and the ratio of Bax/Bcl-xL was dose-dependently ...
Keywords: فاکتور رشد اندوتلیال عروقی (VEGF); AP-1; activator protein-1; Bax; Bcl-2-associated X protein; Bcl-2; B cell lymphoma ... C/EBP-homologous protein 10; DNA; dezoxiribonucleic acid; FITC; fluorescein isothiocyanate; GAPDH; (Glyceraldehyde 3-phosphate ... Keywords: فاکتور رشد اندوتلیال عروقی (VEGF); AMPK; AMP-activated protein kinase; ARF6; ADP-ribosylation factor 6; AKT; protein ... autophagy protein; BAK; Bcl 2 homologous antagonist/killer; BAX; Bcl-2 associated -X protein; Bcl-2; B- ...
2. However, to our knowledge, mitochondrial double-stranded RNA has not been previously characterized in vivo. Here we describe ... bcl-2 Homologous Antagonist-Killer Protein, bcl-2-Associated X Protein ... 2. However, to our knowledge, mitochondrial double-stranded RNA has not been previously characterized in vivo. Here we describe ...
Fas-associated protein with death domatin (FADD), Bcl-2 homologous antagonist killer (BAK), Bcl-2 associated X protein (BAX) ... protein kinase C (PKC), protein kinase R (PKR) and toll-like receptors (TLRs). Accordingly, family members of the innate immune ... Collectively, fluorescent reporter proteins are commonly used in biological studies to image cellular compartments, whole cells ... Among these transcription factors are a family of genes known as Paired box (PAX). PAX proteins are essential in early ...
... homologous antagonist killer (Bak), BCL-2-associated X protein (Bax), and cytochrome c at both the mRNA and protein levels were ... and MCP-1 protein expression, increase IκB protein expression in HPASMCs. According to what we observed, this study indicated ... and increased cell cycle inhibitor proteins p21. Besides, ASE decreased the total protein level of epidermal growth factor ... At the cellular and molecular levels, we found that 18β-GA could significantly reduce the accumulation of misfolded protein in ...
... bcl-X protein - metabolism. Charakt. formalna: Zagraniczny artyku Charakt. merytoryczna: Praca oryginalna. J zyk publikacji: ... Tytu orygina u: Coexistence of homologous-type cervical carcinosarcoma with endometrioid-type G1 endometrial cancer: a case ... bcl-X protein - metabolism. Charakt. formalna: Zagraniczny artyku Charakt. merytoryczna: Praca oryginalna. J zyk publikacji: ... bcl-X protein - metabolism. Charakt. formalna: Zagraniczny artyku Charakt. merytoryczna: Praca oryginalna. J zyk publikacji: ...
bcl2-Antagonist of Cell Death Protein. *bcl2 Antagonist of Cell Death Protein ... "bcl-Associated Death Protein" by people in this website by year, and whether "bcl-Associated Death Protein" was a major or ... A pro-apoptotic protein and member of the Bcl-2 protein family that is regulated by PHOSPHORYLATION. Unphosphorylated Bad ... "bcl-Associated Death Protein" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH ( ...
Direct interaction of the mitochondrial membrane protein carnitine palmitoyltransferase I with Bcl-2. Biochem Biophys Res ... Clinical safety and activity of AG-120, a first-in-class, potent inhibitor of the IDH1 mutant protein, in a phase 1 study of ... Protein synthesis is resistant to rapamycin and constitutes a promising therapeutic target in acute myeloid leukemia. Blood. ... BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells. Cell Stem ...
... bcl-X protein - metabolism ; Proto-oncogene proteins c-bcl-2 - metabolism ; Blotting, Western. Charakt. formalna: Zagraniczne ... Angielskie s owa kluczowe: Graves disease - pathology ; Goiter, nodular - pathology ; Proto-oncogene proteins c-bcl-2 - ... Tytu orygina u: Identification of proapoptotic (BAK,BAX) and antiapoptotic (BCL-xL), BCL-2) proteins in thyrocytes from ... Proto-oncogene proteins c-bcl-2 - biosynthesis ; Thyrotropin - blood ; Thyroxine - blood ; Triiodothyronine - blood. Charakt. ...
Expression of WAVEs, the WASP (Wiskott-Aldrich syndrome protein) family of verprolin homologous proteins in human wound tissues ... The role of Bik1 (BCL-2 interaction killer) in wound healing [Abstract]. Wound Repair and Regeneration 18(6), pp. A92. (10.1111 ... for resistance and recurrence after conventional chemotherapy and also the recently introduced smoothened antagonists. ... Expression of WAVEs, the WASP (Wiskott-Aldrich syndrome protein) family of verprolin homologous proteins in human wound tissues ...
... protein-coding genes corresponding to TFs (from TransmiR), and signaling proteins (from TransmiR). The triangle denotes the ... Guirouilh-Barbat JK, Wilhelm T, Lopez BS: AKT1/BRCA1 in the control of homologous recombination and genetic stability: the ... MicroRNA-125b confers the resistance of breast cancer cells to paclitaxel through suppression of pro-apoptotic Bcl-2 antagonist ... killer 1 (Bak1) expression. J Biol Chem. 2010, 285: 21496-21507. 10.1074/jbc.M109.083337. ...
Many viruses encode proteins that can inhibit apoptosis.[104] Several viruses encode viral homologs of Bcl-2. These homologs ... such as Natural Killer and cytotoxic T cells) that then induce the infected cell to undergo apoptosis.[99] ... The adenovirus E1B-55K protein and the hepatitis B virus HBx protein are examples of viral proteins that can perform such a ... these inhibitory proteins target retinoblastoma tumor-suppressing proteins.[84] These tumor-suppressing proteins regulate the ...
Protein metabolism ‎]] #[[Prozone ‎]] #[[Robert W. Holley ‎]] #[[Röntgen equivalent man ‎]] #[[SUMO protein ‎]] #[[ ... Homologous series ‎]] #[[ICD-10 Chapter K ‎]] #[[Cementum ‎]] #[[Chronic stable angina historical perspective ‎]] #[[Cluster of ... Antagonist (muscle) ‎]] #[[Anti-ganglioside antibodies ‎]] #[[Arcuate vein ‎]] #[[Arene substitution patterns ‎]] #[[ATC code H ... Natural Killer T cell ‎]] #[[Dichloromethane ‎]] #[[Extensor hallucis longus muscle ‎]] #[[Exudate ‎]] #[[Failure to thrive ...
Ajuba, a novel LIM protein, interacts with Grb2, augments mitogen- activated protein kinase activity in fibroblasts, and ... Natural killer cells from HIV-1+ patients produce C-C chemokines and inhibit HIV-1 infection. Fehniger, T. A., Herbein, G., Yu ... bcl-2 gene rearrangement determined by PCR as a mean to detect minimal residual disease in malignant lymphomas. Xiang, Z. F., ... Peptidomimetic antagonist of the integrin α(v)β3 inhibits leydig cell tumor growth and the development of hypercalcemia of ...
BCL2 Antagonist/Killer 1) ELISA Kit based in Delhi, India ... Rat BAK1(BCL2 Antagonist/Killer 1) ELISA Kit. *Rat BAX(BCL-2 ... Rat SP-A1(Pulmonary surfactant-associated protein A1) ELISA Kit. *Rat SP-A1(Pulmonary surfactant-associated protein A1) ELISA ... Rat BAK1(BCL2 Antagonist/Killer 1) ELISA Kit Synonyms:BAK, BAK-LIKE, BCL2L7, CDN1, Bcl-2 Homologous Antagonist/Killer. Intended ... Get a price quote for Rat BAK1(BCL2 Antagonist/Killer 1) ELISA Kit ...
Sperm postacrosomal WW domain-binding protein is not required for mouse egg activation. C/EBP homologous protein deficiency ... Bcl-xL Displays Restricted Distribution during T Cell Developement and Inhibits Multiple Forms of Apoptosis but Not Clonal ... T Cell Receptor Antagonist Peptides Induce Positive Selection. Tissue-specific knockout of the mouse Pig-a gene reveals ... Reversible Defects in Natural Killer and Memory CD8 T Cell Lineages in Interleukin 15-deficient Mice. Differential T Cell ...
BH3-only proteins of the Bcl-2 family, Bim and Puma, are required for the initiation of apoptosis by multiple stimuli, ... To confirm that Dex-dependent cell death and E4BP4 and Bim upregulation are dependent on GR, the effects of the GR antagonist ... E4BP4 has been shown to induce differentiation in monocyte-macrophages [50], to drive natural killer cell lineage development [ ... The mouse and human E4BP4 genes are highly homologous, with 79% nucleotide sequence identity in the coding region. The two ...
B cell lymphoma 6 protein (BCL-6), was identified183,184,185. TFH cells represent a specialized subset of CD4+ T cells that ... Self-amplifying mRNA vaccines expressing multiple conserved influenza antigens confer protection against homologous and ... antagonist increased the cytolytic capacity of CD8+ T cells and modestly delayed tumour growth in OVA-expressing lymphoma or ... Tumor associated antigen and interleukin-12 mRNA transfected dendritic cells enhance effector function of natural killer cells ...
Martens C, Bilodeau S, Maira M, Gauthier Y, Drouin J. (2005) Protein-protein interactions and transcriptional antagonism ... Antagonist Comments. Based on alignment with the related NR4A subfamilly members and on 3D structure analysis of the LBD, NR4A1 ... 2004) Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3. Cell, 116 (4): 527-40 ... 1990) A human early response gene homologous to murine nur77 and rat NGFI-B, and related to the nuclear receptor superfamily. ...
PA can induce the expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein ( ... Colchicine is also a competitive antagonist of the α3 glycine receptors (GlyRs). ... Natural Killer Group 2, Member D (NKG2D). *Prostate Specific Membrane Antigen. *CRACC/SLAMF7 ... Viral Proteins. Biotinylated Proteins. Fluorescent-labeled Proteins. GMP-grade Proteins. Animal-free Recombinant Proteins. ...
antagonist blocks histamine-induced proinflammatory cytokine production through inhibition of Ca2+-dependent protein kinase C, ... Regulation of expression of Bcl-3 proto-oncogene by IKK ϵ. *Regulation of I-kappa-B kinase (IKK) Pathway by CARMA 1• Bcl-10• ... IKK-i and TBK-1 are Enzymatically Distinct from the Homologous Enzyme IKK-2 COMPARATIVE ANALYSIS OF RECOMBINANT HUMAN IKK-i, ... Deficient natural killer cell cytotoxicity in patients with IKK-γ/NEMO mutations ...
... promotes cancer metastasis through resistance to anoikis and increased invasiveness Co-targeting of BAX and BCL-XL proteins ... Reparative effects of interleukin-1 receptor antagonist in young and aged/co-morbid rodents after cerebral ischemia Epithelial- ... pylori infection in a pig model is dominated by Th1 and cytotoxic CD8+ T cell responses Epigenetic control of natural killer ... microtissue and its application for adverse drug reaction assay Non-catalytic roles for XPG with BRCA1 and BRCA2 in homologous ...
Protein fabrication automation. * Protein isoforms encoded by the pX region of human T-cell leukemia/lymphotropic virus type I. ... Frequent detection of bcl-2/JH translocations in human blood and organ samples by a quantitative polymerase chain reaction ... Identification and mapping of type 1 neurofibromatosis (NF1) homologous loci. * Identification of Aedes aegypti and its ... cDNA cloning of an intracellular form of the human interleukin 1 receptor antagonist associated with epithelium. ...
... protein flare C SCANS studie C-486 C-ALCL C-ETACs as hallmarks of cancer C-ion RT C-reactive protein C-reactive protein ... BBD-BC BCBM BCC BCCs BCCSS BCG BCG vaccination in childhood BCG-unresponsive non-muscle-invasive bladder cancer BCIN+ BCIS Bcl- ... agonists versus GnRH antagonists CVD risk factors CVD risk factors and colorectal cancer CVEs CVSS-studie CXB CXCL8-CXCR1 2 ... levels cytokine-induced killer cell therapy cytokines cytology testing cytoreductive surgery Cytosponge-trefoil factor 3 D-2- ...
  • Natural substances exert their anti-cancer activity by modulating cell cycle progression and inducing apoptosis-regulatory proteins ( 8 , 9 ). (spandidos-publications.com)
  • Many viruses express antiapoptotic proteins to counter host defense mechanisms that would otherwise trigger the rapid clearance of infected cells. (nih.gov)
  • In addition, B-cell lymphoma (Bcl)-2 family proteins are important for apoptosis regulation, which could be either proapoptotic, such as Bcl-2-associated X protein (Bax) or Bcl-2 homologous antagonist/killer, or antiapoptotic, such as Bcl-2 and Bcl-extra large (Bcl-xL) ( 13 ). (spandidos-publications.com)
  • PA can induce the expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in in mouse granulosa cells. (medchemexpress.com)
  • This protein localizes to mitochondria, and functions to induce apoptosis. (wikipedia.org)
  • Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN. (ucdenver.edu)
  • Sulindac sulfide inhibits epidermal growth factor-induced phosphorylation of extracellular-regulated kinase 1/2 and Bad in human colon cancer cells. (ucdenver.edu)
  • Sulforaphane increases tumor suppressor protein transcription and inhibits histone deacetylase activity. (medchemexpress.com)
  • Epigallocatechin Gallate inhibits glutamate dehydrogenase 1/2 (GDH1/2, GLUD1/2) activity. (medchemexpress.com)
  • Novel benzylidene-thiazolidine-2,4-diones inhibit Pim protein kinase activity and induce cell cycle arrest in leukemia and prostate cancer cells. (ucdenver.edu)
  • Some factors like Fas receptors and caspases promote apoptosis, while some members of the Bcl-2 family of proteins inhibit apoptosis. (mdwiki.org)
  • [5] Both pathways induce cell death by activating caspases , which are proteases , or enzymes that degrade proteins. (mdwiki.org)
  • The two pathways both activate initiator caspases, which then activate executioner caspases, which then kill the cell by degrading proteins indiscriminately. (mdwiki.org)
  • Bcl-2 homologous antagonist/killer is a protein that in humans is encoded by the BAK1 gene on chromosome 6. (wikipedia.org)
  • BAK1 is a pro-apoptotic Bcl-2 protein containing four Bcl-2 homology (BH) domains: BH1, BH2, BH3, and BH4. (wikipedia.org)
  • As a member of the BCL2 protein family, BAK1 functions as a pro-apoptotic regulator involved in a wide variety of cellular activities. (wikipedia.org)
  • The inactive form of BAK1 is maintained by the protein's interactions with VDAC2, Mtx2, and other anti-apoptotic members of the BCL2 protein family. (wikipedia.org)
  • The protein encoded by this gene belongs to the BCL2 protein family. (wikipedia.org)
  • This occurred in 1988 when it was shown that BCL2, the gene responsible for follicular lymphoma, encoded a protein that inhibited cell death. (mdwiki.org)
  • This protein also interacts with the tumor suppressor P53 after exposure to cell stress. (wikipedia.org)
  • This mainly results from the high frequency of distant relapses caused by tumor regrowth initiated by chemoresistant leukemic clones after chemotherapy [ 2 , 3 ]. (biomedcentral.com)
  • The first report of the successful use of in vitro transcribed (IVT) mRNA in animals was published in 1990, when reporter gene mRNAs were injected into mice and protein production was detected 5 . (nature.com)
  • Comparison of E-cadherin with STAT3 and apoptosis regulators: Bak and Bcl-xL in endometrioid adenocarcinomas of different ER-alpha immunoprofile. (edu.pl)
  • Here, we identify Nfat proteins as Sox10 targets and regulators of oligodendroglial differentiation in rodents and humans. (regenerativemedicine.net)
  • In addition, FCP induced caspase‑3 activation and subsequent PARP cleavage, and increased the B‑cell lymphoma (Bcl)‑2‑associated X protein/Bcl‑extra large ratio in A549 cells. (spandidos-publications.com)
  • These findings expand the family of protein sequences that act like Bcl-2 to block apoptosis and support the conclusion that the prosurvival action of these proteins critically depends on their ability to bind and antagonize Bax and/or Bak. (nih.gov)
  • A pro-apoptotic protein and member of the Bcl-2 protein family that is regulated by PHOSPHORYLATION. (ucdenver.edu)
  • Neuronal apoptosis induced by selective inhibition of Rac GTPase versus global suppression of Rho family GTPases is mediated by alterations in distinct mitogen-activated protein kinase signaling cascades. (ucdenver.edu)
  • Upregulation of the BH3-only member of Bcl-2 family proteins, Bim, has been shown to be essential for GC-evoked apoptosis of leukemic lymphoblasts. (jmolecularsignaling.com)
  • On a molecular level, Nfat proteins cooperate with Sox10 to relieve reciprocal repression of Olig2 and Nkx2.2 as precondition for oligodendroglial differentiation and myelination. (regenerativemedicine.net)
  • Research has proven that mRNA mimetics have superior translational efficiency than recombinant DNA and, unlike recombinant proteins, can be endogenously modified in vivo. (pharna.com)
  • Meshki J, Caino MC, von Burstin VA, Griner E, Kazanietz MG. Regulation of prostate cancer cell survival by protein kinase Cepsilon involves bad phosphorylation and modulation of the TNFalpha/JNK pathway. (ucdenver.edu)
  • Protein disulfide isomerase homolog PDILT is required for quality control of sperm membrane protein ADAM3 and male fertility [corrected]. (kumamoto-u.ac.jp)
  • Yan B, Zemskova M, Holder S, Chin V, Kraft A, Koskinen PJ, Lilly M. The PIM-2 kinase phosphorylates BAD on serine 112 and reverses BAD-induced cell death. (ucdenver.edu)
  • For example, adenoviruses and some gamma-herpesviruses express homologs of prosurvival Bcl-2 to subvert the host's apoptotic machinery. (nih.gov)
  • The growth factors in medical use so far have been produced using recombinant DNA or recombinant protein approaches. (pharna.com)
  • Recent improvements in mRNA vaccines act to increase protein translation, modulate innate and adaptive immunogenicity and improve delivery. (nature.com)
  • Over the past decade, major technological innovation and research investment have enabled mRNA to become a promising therapeutic tool in the fields of vaccine development and protein replacement therapy. (nature.com)
  • Consequently, in mammals, mitochondrial DNA is subjected to bidirectional transcription that generates overlapping transcripts, which are capable of forming long double-stranded RNA structures1,2. (ox.ac.uk)
  • Characterization of the murine cytomegalovirus early transcription unit e1 that is induced by immediate-early proteins. (kumamoto-u.ac.jp)
  • bcl-Associated Death Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ucdenver.edu)
  • This graph shows the total number of publications written about "bcl-Associated Death Protein" by people in this website by year, and whether "bcl-Associated Death Protein" was a major or minor topic of these publications. (ucdenver.edu)
  • Below are the most recent publications written about "bcl-Associated Death Protein" by people in Profiles. (ucdenver.edu)
  • Death-effector domain-containing protein DEDD is an inhibitor of mitotic Cdk1/cyclin B1. (kumamoto-u.ac.jp)
  • A hydrophobic groove formed along the C-terminal of α2 to the N-terminal of α5, and some residues from α8, binds the BH3 domain of other BCL-2 proteins in its active form. (wikipedia.org)
  • Nur77 binding induces a Bcl-2 conformational change that exposes its BH3 domain, resulting in conversion of Bcl-2 from a protector to a killer. (guidetopharmacology.org)
  • NR4A1 seems to interact with SRC-2 via its a/B domain. (guidetopharmacology.org)
  • SRC-2 modulates the activity of the N-terminal AF-1 domain. (guidetopharmacology.org)
  • In cardiovascular research, growth factors such as VEGF have been used as ligands to stimulate angiogenesis whereas in cancer research inhibition of dysregulated growth factor receptors is the premise for several clinically used drugs including inhibitors of VEGF receptor (VEGFR), EGR receptor 1 (HER1), and EGF receptor 2 (HER2). (pharna.com)
  • NFAT proteins are also detected in human oligodendrocytes, downregulated in active multiple sclerosis lesions and thus likely relevant in demyelinating disease. (regenerativemedicine.net)
  • Analysis of its three-dimensional structure reveals that despite lacking any primary sequence similarity to Bcl-2, it adopts a virtually identical protein fold. (nih.gov)
  • Coexistence of homologous-type cervical carcinosarcoma with endometrioid-type G1 endometrial cancer: a case report with an immunohistochemical study. (edu.pl)