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.
A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.
Cell-surface receptors that bind LEUKOTRIENES with high affinity and trigger intracellular changes influencing the behavior of cells. The leukotriene receptor subtypes have been tentatively named according to their affinities for the endogenous leukotrienes LTB4; LTC4; LTD4; and LTE4.
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.
Derivatives of ACETIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxymethane structure.
Drugs that are used to treat asthma.
Tumors or cancer of the LUNG.
The B-cell leukemia/lymphoma-2 genes, responsible for blocking apoptosis in normal cells, and associated with follicular lymphoma when overexpressed. Overexpression results from the t(14;18) translocation. The human c-bcl-2 gene is located at 18q24 on the long arm of chromosome 18.
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).
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.
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.
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.
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.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A protein that has been shown to function as a calcium-regulated transcription factor as well as a substrate for depolarization-activated CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. This protein functions to integrate both calcium and cAMP signals.
Tumors or cancer of the COLON.
Human COLORECTAL CARCINOMA cell line.
A cell line derived from cultured tumor cells.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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.
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
An oxidoreductase that catalyzes the reaction between superoxide anions and hydrogen to yield molecular oxygen and hydrogen peroxide. The enzyme protects the cell against dangerous levels of superoxide. EC 1.15.1.1.
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)
Neurons which activate MUSCLE CELLS.
A multifunctional heterogeneous-nuclear ribonucleoprotein that may play a role in homologous DNA pairing and recombination. The N-terminal portion of protein is a potent transcriptional activator, while the C terminus is required for RNA binding. The name FUS refers to the fact that genetic recombination events result in fusion oncogene proteins (ONCOGENE PROTEINS, FUSION) that contain the N-terminal region of this protein. These fusion proteins have been found in myxoid liposarcoma (LIPOSARCOMA, MYXOID) and acute myeloid leukemia.

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。
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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Doç. Dr. Uğur Aydın kim olduğunu ve kısa biyografisi burada bulabilir, hangi hastanede çalıştığına bakıp hemen randevu oluşturabilirsiniz.
Doç.Dr. BURAK ÖZKAN; Bakırköy Hastanesi lokasyonunda Üroloji bölümünde çalışmaktadır. Bilgi ve randevu için tıklayın.
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 ...
Bakırköy Mac Tamiri olarak 2003 senesinden günümüze profesyonel, güler yüzlü ve en uygun fiyatlı Mac Tamiri hizmeti vermekteyiz. Sizlerde Kurumsal bir bilgisayar servisi ile çalışmak istiyorsanız, EN UYGUN fiyatlı ve EN HIZLIRead More…. ...
Diş həkimi Fərid Zeynalov. Dental Expert stomatoloji klinika, Bakı Azərbaycan, Avrasiya Hospital, Dental One, Pulpa Dent, MediStyle, InterMed
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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 ...
Lurer du på hvordan Paradise Hotell fungerer bak kulissene? Eller hvordan Ex on the Beach-deltakerne ble funnet?. Liza Priestley har jobbet som castingansvarlig på en rekke realityproduksjoner opp gjennom årene, og kommer til Amandusfestivalen for å gi et innblikk i hvordan reality-TV fungerer bak kamera.. Bilde: TV 3. ...
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Doç. Dr. Özgür Samancılar kim olduğunu ve kısa biyografisi burada bulabilir, hangi hastanede çalıştığına bakıp hemen randevu oluşturabilirsiniz.
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TY - JOUR. T1 - E6 proteins from multiple human betapapillomavirus types degrade bak and protect keratinocytes from apoptosis after UVB irradiation. AU - Underbrink, Michael P.. AU - Howie, Heather L.. AU - Bedard, Kristin M.. AU - Koop, Jennifer I.. AU - Galloway, Denise A.. PY - 2008/11/1. Y1 - 2008/11/1. N2 - Human papillomavirus (HPV) types from the beta genus (beta-HPVs) have been implicated in the development of skin cancer. A potentially important aspect of their carcinogenic role is the ability of the E6 protein to degrade the proapoptotic family member Bak, which gives cells the ability to survive UV damage. However, it is unknown if the ability to degrade Bak is limited to certain beta-HPV types or whether E6 expression in keratinocytes affects other proteins important for apoptosis signaling. We tested the abilities of E6 proteins from several representative members of the beta-HPVs to degrade Bak and protect UV-treated keratinocytes from apoptosis. The E6 proteins of the beta-HPV ...
TY - JOUR. T1 - Type I Interferon Upregulates Bak and Contributes to T Cell Loss during Human Immunodeficiency Virus (HIV) Infection. AU - Fraietta, Joseph A.. AU - Mueller, Yvonne M.. AU - Yang, Guibin. AU - Boesteanu, Alina C.. AU - Gracias, Donald T.. AU - Do, Duc H.. AU - Hope, Jennifer L.. AU - Kathuria, Noshin. AU - McGettigan, Shannon E.. AU - Lewis, Mark G.. AU - Giavedoni, Luis D.. AU - Jacobson, Jeffrey M.. AU - Katsikis, Peter D.. N1 - Copyright: Copyright 2013 Elsevier B.V., All rights reserved.. PY - 2013/10. Y1 - 2013/10. N2 - The role of Type I interferon (IFN) during pathogenic HIV and SIV infections remains unclear, with conflicting observations suggesting protective versus immunopathological effects. We therefore examined the effect of IFNα/β on T cell death and viremia in HIV infection. Ex vivo analysis of eight pro- and anti-apoptotic molecules in chronic HIV-1 infection revealed that pro-apoptotic Bak was increased in CD4+ T cells and correlated directly with sensitivity ...
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 ...
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 ...
The BCL2 oncogene is a potent suppressor of apoptosis under diverse conditions. BAK1, a gene belonging to the BCL2 family, promotes cell death and counteracts the protection from apoptosis provided by BCL2 [2198]. Bak knockout mice showed reduced age-related apoptotic cell death of spiral ganglion neurons and hair cells in the cochlea, which in turn resulted in the prevention of age-related hearing loss [2200]. ...
Chen M., Huang L., Shabier Z., Wang J.. The lifespan of dendritic cells (DCs) can potentially influence immune responses by affecting the duration of DCs in stimulating lymphocytes. Significant differences in the lifespan have been reported for various DC subsets, however, the molecular mechanisms for regulating such differences between DC subsets remain unclear. In this study, we compared the apoptosis signaling molecules in two major DC subjects, the myeloid DCs (mDCs) and plasmacytoid DCs (pDCs). We observed a lower ratio between anti-apoptotic Bcl-2/Bcl-xL and pro-apoptotic Bax/Bak in shorter-lived myeloid DCs (mDCs) than in longer-lived plasmacytoid DCs (pDCs) or T cells. Transfection with Bcl-2 or Bcl-xL prolonged the survival of mouse primary mDCs in vitro, while deletion of Bcl-2 accelerated DC turnover in vivo. In addition, the ratios between anti-apoptotic Bcl-2/Bcl-xL and pro-apoptotic Bax/Bak could be regulated in DCs. Signaling from toll-like receptors (TLRs) up-regulated Bcl-xL and ...
The power of interferons (IFNs) to inhibit viral replication and cellular proliferation is well established but the specific contribution of each IFN-stimulated gene (ISG) to these biological responses remains to be completely understood. In addition ISG54 was not able to promote cell death in the absence of pro-apoptotic Bcl family members Bax and Bak. Analyses of binding partners of ISG54 uncovered association with two homologous protein ISG56/IFIT1 and ISG60/IFIT3. Furthermore ISG60 binding regulates the apoptotic ramifications of GDC-0973 ISG54 negatively. The outcomes reveal a previously unidentified function of ISG54 in the induction of apoptosis with a mitochondrial pathway and shed brand-new light over the mechanism where IFN elicits anti-viral and anti-cancer results. (6). Still a primary hyperlink of ISGs to mitochondrial-mediated cell loss of life continues to be to become characterized. Within this survey we recognize ISG54 being a GDC-0973 mediator of mitochondrial cell loss of ...
A u Zaw Lin Aung nih an thawngpang an theih bak cun an va zoh i, Myo Lwin Oo i a nupi cu arak thi cang. An ihkhun ah thihnai he a ruak in a rak um. An khuachung upa pawl he Maubin Township palik sinah buainak cu an chuahpi i lainawng tu cu an tleih. A nupi a thah nak ruang cu an hal i padang a chawnh ruang ah a si a ti. thehlut ih tualthattu cu an kai. A chawnh mi pa cu a tlangval maw, zeiruang ah dah a chawnh timi cu an langhter rih loh.. ...
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Bitkisel ve Hayvansal Yetiştiricilik, Hastalıkları, Zararlıları, Besin Noksanlıkları, Kanunları, Desteklemeleri, Mutfakta ve Sanayide kullanımı, Tarım marketi, Tarım Market
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Carreras, L. (Ophavsmand), Turon, A. (Ophavsmand), Bak, B. L. V. (Ophavsmand), Lindgaard, E. (Ophavsmand), Renart, J. (Ophavsmand), de la Escalera, F. M. (Ophavsmand) & Essa, Y. (Ophavsmand), Mendeley Data, 13 dec. 2018. DOI: 10.17632/87r49xbrp3.1, https://data.mendeley.com/datasets/87r49xbrp3/1. Datasæt ...
... by inhibiting the apoptosis-causing proteins, Bcl-2-associated X protein and Bcl-2 homologous antagonist killer. BCL6: This ... 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, ... GSK525762, an inhibitor of the BET family of proteins, suppresses expression of the MYC gene and is undergoing a phase I ...
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- ...
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, ... "Reversible Photocontrol of DNA Binding by a Designed GCN4-bZIP Protein". Biochemistry. 45 (19): 6075-6084. CiteSeerX 10.1.1.555 ...
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 ...
protein binding. • heme binding. • electron carrier activity. Cellular component. • cytosol. • protein phosphatase type 2A ... BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... Soltys BJ, Gupta RS (2000). "Mitochondrial proteins at unexpected cellular locations: export of proteins from mitochondria from ... "Effect of constitutive 70-kDa heat shock protein polymerization on its interaction with protein substrate". The Journal of ...
"Fas-mediated apoptosis in neuroblastoma requires mitochondrial activation and is inhibited by FLICE inhibitor protein and Bcl-2 ... natural killer cell activation. • negative regulation of I-kappaB kinase/NF-kappaB signaling. • TRAIL-activated apoptotic ... protein complex binding. • scaffold protein binding. • protein binding. • identical protein binding. • cysteine-type ... The N-terminal FADD-like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD ...
Many viruses encode proteins that can inhibit apoptosis.[94] Several viruses encode viral homologs of Bcl-2. These homologs can ... such as Natural Killer and cytotoxic T cells) that then induce the infected cell to undergo apoptosis.[89] ... 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.[74] These tumor-suppressing proteins regulate the ...
Bcl-Xl ಮತ್ತು Bcl-2 ) ಸದಸ್ಯರ ನಡುವಿನ ಒಂದು ಸಮತೋಲನವು ಸ್ಥಾಪನೆಗೊಳ್ಳುತ್ತದೆ. ಈ ಸಮತೋಲನವು ಅಪೊಪ್ಟೋಟಿಕ್‌-ಪರವಾದ ಹೋಮೋಡೈಮರ್‌ಗಳ ಪ್ರಮಾಣ ಅಥವಾ ... "Sequential degradation of proteins from the nuclear envelope during apoptosis". Journal of Cell Science. 114 (20): 3643-53. ... BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... ವೈರಾಣುವಿನ Bcl-2 ಪ್ರೊಟೀನುಗಳ ಉದಾಹರಣೆಗಳಲ್ಲಿ ಎಪ್‌ಸ್ಟೀನ್‌-ಬಾರ್‌ ವೈರಾಣು BHRF1 ಪ್ರೊಟೀನು ಮತ್ತು ಅಡಿನೋವೈರಸ್‌ E1B 19K ಪ್ರೊಟೀನು ಸೇರಿವೆ.[೪೩] ...
... which is facilitated by binding to adaptor proteins via protein-protein interaction motifs that are collectively referred to as ... BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... 7 (2): 99-109. doi:10.1038/nrmicro2070. PMC 2910423. PMID 19148178.. *^ a b c d e f Eldridge, Matthew JG; Shenoy, Avinash R ( ... The adaptor protein FADD will recruit (by a Death domain-Death domain interaction) pro-Caspase 8 via the DED domain. This FasR ...
... which is facilitated by binding to adaptor proteins via protein-protein interaction motifs that are collectively referred to as ... BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... 7 (2): 99-109. doi:10.1038/nrmicro2070. PMC 2910423 . PMID 19148178.. *^ a b c d e f Eldridge, Matthew JG; Shenoy, Avinash R. " ... The adaptor protein FADD will recruit (by a Death domain-Death domain interaction). The other end of the adaptor contains a DED ...
Many viruses encode proteins that can inhibit apoptosis.[103] 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.[98] ... 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.[83] These tumor-suppressing proteins regulate the ...
... to allow unambiguous identification of a protein.,p>,a href=/help/protein_names target=_top>More...,/a>,/p>Protein namesi. ... heat shock protein binding Source: Ensembl. *identical protein binding Source: UniProtKBInferred from physical interactioni*. " ... Protein family/group databases. TCDBi. 1.A.21.1.3, the bcl-2 (bcl-2) family. ... PROSITE; a protein domain and family database. More...PROSITEi. View protein in PROSITE. PS50062, BCL2_FAMILY, 1 hit. PS01080 ...
The Bcl-2 family of proteins includes the major regulators and effectors of the intrinsic apoptosis pathway. Cancers are ... structure of a photoswitchable peptide derived from the proapoptotic protein Bak in complex with the antiapoptotic protein Bcl- ... NMR solution structure of a photoswitchable apoptosis activating Bak peptide bound to Bcl-xL J Am Chem Soc. 2012 May 9;134(18): ... The Bcl-2 family of proteins includes the major regulators and effectors of the intrinsic apoptosis pathway. Cancers are ...
The expression of the cell death-inducing protein, Bak, was investigated in 41 cases of Hodgkins disease and was correlated ... bcl-2 Homologous Antagonist-Killer Protein Grant support * CA-60421-02/CA/NCI NIH HHS/United States ... Detection of the cell death-inducing protein BAK in Reed-Sternberg cells of Hodgkins disease Leuk Lymphoma. 1999 Aug;34(5-6): ... The expression of the cell death-inducing protein, Bak, was investigated in 41 cases of Hodgkins disease and was correlated ...
Protein Ontology. PR:000002185 bcl-2 homologous antagonist/killer. (term hierarchy). * PDB ... J:43660 Chittenden T, et al., A conserved domain in Bak, distinct from BH1 and BH2, mediates cell death and protein binding ... IPR020717 Apoptosis regulator, Bcl-2, BH1 motif, conserved site. IPR020726 Apoptosis regulator, Bcl-2, BH2 motif, conserved ... 3 phenotypes from 1 allele in 2 genetic backgrounds 51 phenotypes from multigenic genotypes 119 phenotype references ...
Protein Coding), BCL2 Antagonist/Killer 1, including: function, proteins, disorders, pathways, orthologs, and expression. ... Protein details for BAK1 Gene (UniProtKB/Swiss-Prot). Protein Symbol:. Q16611-BAK_HUMAN. Recommended name:. Bcl-2 homologous ... BAK1 (BCL2 Antagonist/Killer 1) is a Protein Coding gene. Diseases associated with BAK1 include Absolute Glaucoma and ... The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act ...
Cardioviruses lack a protein homologous to the enterovirus (e.g., PV and HRV) 2A protease, and instead the NE alterations are ... Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy. Nat Rev Mol Cell Biol15:49-63. doi: ... The leader protein of Theilers virus interferes with nucleocytoplasmic trafficking of cellular proteins. J Virol78:4357-4362. ... Protein kinase Cδ (PKCδ) is a proapoptotic protein that accumulates in the nucleus during apoptosis. Full-length PKCδ is found ...
Proto-Oncogene Proteins c-bcl-2. en. dc.subject. Proto-Oncogene Proteins c-myc. en. ... bcl-2-Associated X Protein. en. dc.title. BAK and NOXA are critical determinants of mitochondrial apoptosis induced by ... The multidomain proapoptotic protein BAK, but not its orthologue BAX, was found to be essential for bortezomib-induced ... bcl-2 Homologous Antagonist-Killer Protein. en. dc.subject. ...
Recently, m41.1, a protein product encoded by the m41 open reading frame (ORF) of MCMV, has been shown to inhibit Bak activity ... The Bcl-2 family of proteins are the principle regulators of apoptosis, with two pro-apoptotic members, Bax and Bak, essential ... Recently, m41.1, a protein product encoded by the m41 open reading frame (ORF) of MCMV, has been shown to inhibit Bak activity ... The Bcl-2 family of proteins are the principle regulators of apoptosis, with two pro-apoptotic members, Bax and Bak, essential ...
These two proteins move to the mitochondrial membrane and disrupt the anti-apoptotic function of the Bcl-2 family proteins, ... 53 kDa protein; PDK-1, phosphoinositide-dependent protein kinase 1; PI3K, phosphoinositide 3-kinase; PKB/Akt, protein kinase B. ... BH3-only proteins, such as Bid, Bim, Bad, Bik, and Puma, which generally possess only the BH3 domain [47]. The Bcl-2 family of ... L -associated death domain protein; Bax, Bcl-2-associated X protein; Bcl-X L , Bcl-2-related gene, long form; Bim, Bcl-2- ...
PBMC were exposed to 105 TCID50/ml HIV-1Ba-L in the presence or absence of a TLR7/9 antagonist for 24 hours (n = 13) and IFNα ... PBMC were exposed to 105 TCID50/ml HIV-1Ba-L in the presence or absence of a TLR7/9 antagonist for 24 hours (n = 13) and IFNα ... B) HIV-1Ba-L exposure increases CD95/Fas apoptosis of T cells, which is inhibited by a TLR7/9 antagonist and anti-IFNα/β ... B) HIV-1Ba-L exposure increases CD95/Fas apoptosis of T cells, which is inhibited by a TLR7/9 antagonist and anti-IFNα/β ...
102389749 BNIP3L; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like isoform X1 102416581 BCL2L1; bcl-2-like protein ... BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 K15465 BNIP3L; BCL2/adenovirus E1B 19 kDa protein-interacting protein ... 102407734 TTYH3; protein tweety homolog 3 isoform X1 102401002 TTYH1; LOW QUALITY PROTEIN: protein tweety homolog 1 102409910 ... 102400842 TMC4; LOW QUALITY PROTEIN: transmembrane channel-like protein 4 102409065 TMEM63A; CSC1-like protein 1 isoform X2 ...
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 ...
... by inhibiting the apoptosis-causing proteins, Bcl-2-associated X protein and Bcl-2 homologous antagonist killer. BCL6: This ... 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, ... GSK525762, an inhibitor of the BET family of proteins, suppresses expression of the MYC gene and is undergoing a phase I ...
RAC serine/threonine-protein kinase [EC:2.7.11.1]. K02158 Bcl-2-antagonist of cell death. ... RAF proto-oncogene serine/threonine-protein kinase [EC:2.7.11.1]. K04368 mitogen-activated protein kinase kinase 1 [EC:2.7.12.2 ... A-Raf proto-oncogene serine/threonine-protein kinase [EC:2.7.11.1]. K04365 B-Raf proto-oncogene serine/threonine-protein kinase ... mitogen-activated protein kinase 8/9/10 (c-Jun N-terminal kinase) [EC:2.7.11.24]. ...
... can lead to apoptotic death via the activation of caspase 3 and the pro-apoptotic proteins BCL-2-associated X protein (BAX) and ... Both pathways have been implicated in phosphorylating and inactivating the pro-apoptotic protein BCL-2-associated agonist of ... AMP-activated protein kinase (AMPK). TSC2 can be directly phosphorylated by both ERK and ERK-activated ribosomal protein S6 ... while upregulating the anti-apoptotic proteins BCL-2 and apoptosis repressor with caspase recruitment domain (ARC). ...
Bcl2 homologous antagonist killer; Bcl2 like 7 Protein; BCL2-antagonist/killer 1; BCL2L7; CDN 1; CDN1; Cell death inhibitor 1; ... FITC ?? Bcl-2ͬԴ?? ?? ??. ??. Apoptosis Regulator Bak; BAK 1; BAK; BAK like; Bak NT; BAK1; Bcl 2 homologous antagonist/killer; ... The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act ... Belongs to the Bcl-2 family.. Subcellular Location:. Mitochondrion membrane.. Tissue Specificity:. Expressed in a wide variety ...
Bcl-2) family member BH3-interacting domain death agonist (BID) to switch on the intrinsic mitochondrial death pathway, leading ... Bcl-2 homologous antagonist/killer- (Bak-) dependent mitochondrial outer membrane permeabilization (MOMP), the dissipation of ... GB activates the proapoptotic B cell CLL/lymphoma 2 ( ... "Natural killer and lymphokine-activated killer cells require ... the nuclear structural protein lamin, the nuclear mitotic apparatus protein (NuMa), the DNA-dependent protein kinase catalytic ...
Montelukast also markedly decreased the phosphorylation of several proteins, such as with no lysine 1 (WNK1), protein kinase B ... Bcl-2), up-regulation of Bcl-2 homologous antagonist/killer (Bak), and nuclear translocation of apoptosis-inducing factor (AIF ... Our previous cohort study showed that cysteinyl leukotriene receptor antagonists, mainly montelukast, decreased the lung cancer ... Further investigation showed the down-regulation of B-cell lymphoma 2 ( ...
Characterization of the protein kinase activity of TRPM7/ChaK1, a protein kinase fused to the transient receptor potential ion ... Thrombin-receptor antagonist vorapaxar in acute coronary syndromes. N Engl J Med. 2012;366:20-33. doi: 10.1056/NEJMoa1109719.. ... involving Bcl-2-associated X protein/Bcl-2 homologous antagonist killer mediated activation of caspase-9, can also lead to ... The actin-binding protein filamin A functions as an important regulator of platelet activation and shape change. Filamin A ...
Bcl-2 homologous antagonist/killer, Apoptosis regulator BAK, Bcl-2-like protein 7, Bcl2-L-7, BAK1, BAK, BCL2L7, CDN1, MGC3887, ... BAK1 is a member of the BCL2 protein family. The BCL2 family members form oligomers or heterodimers and act as anti- or pro- ... BAK1 antibody was purified from mouse ascitic fluids by protein-G affinity chromatography. ...
Furthermore, angiogenesis-related proteins were also stimulated by vitamin K2. In vivo studies revealed enhanced blood vessel ... This suggests that NF-κB antagonists are useful to reverse cirrhosis induced by sarcopenia. This observation also indicates ... Bcl-2 homologous antagonist/killer, known as Bak, but rather associated with the caspase-transglutaminase related pathway of ... In blood vessels, vitamin K2 diminishes the production of hydroxyapatite by carboxylating matrix-Gla protein, as well as the ...
BAK1 belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic ... This protein also interacts with the tumor suppressor P53 after exposure to cell stress.The protein encoded by this gene ... Alternative names for Bcl-2-like 7 antibody. BAK1, BAK, BCL2L7, Bcl2-L-7, CDN1, Bcl-2 homologous antagonist/killer, Apoptosis ... Background of Bcl-2-like 7 antibody. BAK1 belongs to the BCL2 protein family. BCL2 family members form oligomers or ...
... with prodeath proteins, such as BCL-2 homologous antagonist/killer (BAK), and inhibition with small molecular inhibitors, ... To prove on-target activity, it is important to show that prodeath proteins, such as BAK, are released from MCL-1 after ... During the oncogenic transformation, some cancer cells become reliant on continuous expression of an anti-apoptotic protein, ... called BCL-2 homology domain-3 (BH3) mimetics, selectively kills the cancer cells. MCL-1 is of particular interest as a ...
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 induction of apoptosis. Furthermore, we observed that ATF3 overexpression ... and tight junction protein zonula occludens (ZO)-1. This study suggested that ATF3 may play a dichotomous role in regulation of ... Bcl-2), in colon cancer cells, while overexpression of ATF3 resulted in a dramatic decrease in Bcl-2 protein. ...
The expression of tumor protein p53 (p53), Bcl-2 associated X protein (Bax), Bcl-2 homologous antagonist/killer (Bak), ... Bcl-2) was inhibited, resulting in apoptosis. Moreover, oxidative stress indexes, miR-187-5p, and apoptosis-related genes ... Cytochrome-c (Cyt-c), Caspase-9, Caspase-8, and Caspase-3 was promoted, and the expression of B-cell lymphoma-2 ( ...
... pro-apoptotic protein BAK , Bcl2 homologous antagonist/killer , Bcl-2-like 7 ... Protein level used designations for BAK1 BCL2-like 7 protein , apoptosis regulator BAK , bcl-2 homologous antagonist/killer , ... Images for product: BCL2-Antagonist/killer 1 (BAK1) ELISA Kit Diagramm of the ELISA kit to detect Human BAK1with the optical ... Images for product: BCL2-Antagonist/killer 1 (BAK1) ELISA Kit Diagramm of the ELISA kit to detect Human BAK1with the optical ...
Specially, the proapoptotic proteins Bax and Bak are sequestered by the anti-apoptotic proteins Bcl-2, Mcl-1, and Bcl-Xl. Bcl- ... Furthermore, the use of mitochondria-targeted ATPase antagonists is sufficient to block the protection provided by HSP90 and to ... J proteins are chaperones that cooperate with heat shock protein 70 (HSP70) to direct proteins to specific intracellular ... Mediation of the antiapoptotic activity of Bcl-xL protein upon interaction with VDAC1 protein. J Biol Chem (2012) 287:23152-61 ...
Here we show that Bak protein has a much higher affinity than the 26-amino acid Bak Bcl-2 homology domain 3 for Bcl-2, that ... Here we show that Bak protein has a much higher affinity than the 26-amino acid Bak Bcl-2 homology domain 3 for Bcl-2, that ... Here we show that Bak protein has a much higher affinity than the 26-amino acid Bak Bcl-2 homology domain 3 for Bcl-2, that ... Here we show that Bak protein has a much higher affinity than the 26-amino acid Bak Bcl-2 homology domain 3 for Bcl-2, that ...
... levels of phosphorylated-STAT3Tyr705 and the anti-apoptotic protein Bcl-2 but an increased level of pro-apoptotic protein Bax. ... STAT3-related proteins were analysis by western blotting analysis and Immunofluorescence assays. Efficacy evaluation of ATO ... stimulated by interleukin-6 and downregulated STAT3 direct target genes and the anti-apoptotic proteins Bcl-2, XIAP, and ... that ATO combined with CT induced cell apoptosis in Bel-7404 cells and upregulated the activation of apoptosis-related proteins ...
bcl-2 Homologous Antagonist-Killer Protein 19% * Cell Death 17% * Spinal Cord Ventral Horn 16% ...
  • 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)
  • BAK1 (BCL2 Antagonist/Killer 1) is a Protein Coding gene. (genecards.org)
  • Also, signalling through the RAS effectors RASSF1, NORE1, mammalian STE20-like protein kinase 1 (MST1) and JUN N-terminal kinase (JNK) can lead to apoptotic death via the activation of caspase 3 and the pro-apoptotic proteins BCL-2-associated X protein (BAX) and BCL-2-homologous antagonist/killer 1 (BAK1). (nih.gov)
  • BAK1 is a member of the BCL2 protein family. (prospecbio.com)
  • BAK1 antibody was purified from mouse ascitic fluids by protein-G affinity chromatography. (prospecbio.com)
  • BAK1 belongs to the BCL2 protein family. (acris-antibodies.com)
  • Immunohistochemistry (IHC) analyzes of Bak1/2 antibody (Cat. (acris-antibodies.com)
  • Western Blot analysis of BAK1 expression in transfected 293T cell line ( H00000578-T02 ) by BAK1 MaxPab polyclonal antibody.Lane 1: BAK1 transfected lysate(23.40 KDa).Lane 2: Non-transfected lysate. (acris-antibodies.com)
  • The expression level of anti-apoptotic gene BCL-2 and pro-apoptosis gene Bak1 were detected by semi-quantitative RT-PCR. (bvsalud.org)
  • VPA could decrease the expression of BCL-2 gene, but did not show obvious effect on the expression of Bak1. (bvsalud.org)
  • Bcl-2-antagonist/killer 1 (Bak1), a pro-apoptotic gene, was a target gene of miR-125b by software predicts. (bvsalud.org)
  • Our results suggest that BCL-2 homologous antagonist/killer (BAK) protein, encoded by BAK1, plays a crucial role in the pathogenesis of DHF. (cdc.gov)
  • We also found that ATO combined with CT reversed the upregulated expression of phosphorylated-STAT3 Tyr705 stimulated by interleukin-6 and downregulated STAT3 direct target genes and the anti-apoptotic proteins Bcl-2, XIAP, and survivin but obviously upregulated the promoting apoptosis proteins Bak,.In vivo studies showed that ATO combined with CT decreased tumor growth. (biomedcentral.com)
  • 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)
  • 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)
  • 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)
  • 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)
  • Bcl-XS lacks the BH1 and BH2 domains of BCL-XL PROTEIN and it inhibits the ANTI-APOPTOTIC PROTEINS of the bcl-2 protein family. (bvsalud.org)
  • The susceptibility to apoptotic cell death is dependent on the relative level of anti-apoptotic proteins of Bcl-2 family members (Bcl-2, Bcl-x L , Mcl-1) to that of pro-apoptotic proteins of the family (Bad, Bax, Bak, Bok) or the interaction of each protein. (biomedcentral.com)
  • Bcl-2, Bcl-XL, Bcl-W, Mcl-1 and A1 proteins function as anti-apoptotic proteins that inhibit apoptosis, while Bax, Bad, Bid, Bok, Bik and Bak (I swear these names are not made up! (scientificamerican.com)
  • The anti-apoptotic proteins bind to and inactivate the pro-apoptotic proteins in a healthy cell that does not need to die. (scientificamerican.com)
  • Bcl-2 (B-cell lymphoma 2), encoded in humans by the BCL2 gene, is the founding member of the Bcl-2 family of regulator proteins that regulate cell death (apoptosis), by either inhibiting (anti-apoptotic) or inducing (pro-apoptotic) apoptosis. (wikipedia.org)
  • Bcl-2 derives its name from B-cell lymphoma 2, as it is the second member of a range of proteins initially described in chromosomal translocations involving chromosomes 14 and 18 in follicular lymphomas. (wikipedia.org)
  • But simultaneous over-expression of Bcl-2 and the proto-oncogene myc may produce aggressive B-cell malignancies including lymphoma. (wikipedia.org)
  • In follicular lymphoma, a chromosomal translocation commonly occurs between the fourteenth and the eighteenth chromosomes - t(14;18) - which places the Bcl-2 gene from chromosome 18 next to the immunoglobulin heavy chain locus on chromosome 14. (wikipedia.org)
  • GB activates the proapoptotic B cell CLL/lymphoma 2 (Bcl-2) family member BH3-interacting domain death agonist (BID) to switch on the intrinsic mitochondrial death pathway, leading to Bcl-2-associated X protein (Bax)/Bcl-2 homologous antagonist/killer- (Bak-) dependent mitochondrial outer membrane permeabilization (MOMP), the dissipation of mitochondrial transmembrane potential (ΔΨm), and the production of reactive oxygen species (ROS). (hindawi.com)
  • GA cleaves its substrates after lysine or arginine residues to trigger a caspase-independent, B cell CLL/lymphoma 2- (Bcl2-) insensitive, and mitochondrial outer membrane permeabilization- (MOMP-) independent cell death pathway with the morphological feature of apoptosis [ 23 - 27 ]. (hindawi.com)
  • Further investigation showed the down-regulation of B-cell lymphoma 2 (Bcl-2), up-regulation of Bcl-2 homologous antagonist/killer (Bak), and nuclear translocation of apoptosis-inducing factor (AIF) in montelukast-treated lung cancer cells. (mdpi.com)
  • 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. (umd.edu)
  • The expression of tumor protein p53 (p53), Bcl-2 associated X protein (Bax), Bcl-2 homologous antagonist/killer (Bak), Cytochrome- c (Cyt- c ), Caspase-9, Caspase-8, and Caspase-3 was promoted, and the expression of B-cell lymphoma-2 (Bcl-2) was inhibited, resulting in apoptosis. (ovid.com)
  • Additionally, the proapoptotic protein B-cell lymphoma (BCL)-associated X (Bax) can induce loss of the ΔΨmt in a CsA-sensitive manner ( 15 , 16 ). (frontiersin.org)
  • These include malignant tumors that develop in the immunocompromised conditions such as AIDS-associated lymphomas and posttransplant lymphoproliferative disease [ 2 , 3 ] and also several human cancers that develop in the immunocompetent patients such as BL, Hodgkin's lymphoma, B-cell and T-cell lymphomas, epithelial nasopharyngeal carcinoma (NPC), and some forms of gastric carcinomas [ 4 - 6 ]. (hindawi.com)
  • Thus this study was undertaken on Indian children with classical Hodgkin lymphoma to assess the significance of bcl-2, bak and p53 expression, and apoptotic index in relation with EBV status and treatment outcome with chemotherapy alone. (bvsalud.org)
  • Interpretation & conclusion: EBV detection in children with classical Hodgkin lymphoma was associated with significant lower bak expression and with lower spontaneous apoptosis of H-RS cells suggesting that EBV-LMP1 might downregulate bak pro-apoptotic protein. (bvsalud.org)
  • The B-cell lymphoma 2 (Bcl-2) protein family tightly controls activation of the intrinsic pathway. (creative-diagnostics.com)
  • In this review, we describe a number of these mechanisms of chemoresistance including ABC transporter expression, aldehyde dehydrogenase (ALDH) activity, B-cell lymphoma-2 (BCL2) related chemoresistance, enhanced DNA damage response and activation of key signaling pathways. (springeropen.com)
  • Afterwards, cells were lysed and whole proteins lysates were analysed by Western blot for altered expression of X-linked inhibitor of apoptosis protein (XIAP), baculoviral IAP repeat containing 5 (BIRC5), myeloid cell leukemia 1 (MCL1), B-cell lymphoma 2 (BCL2), and BCL2 like 1 (BCL2L1). (thefreedictionary.com)
  • Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma. (rush.edu)
  • Also, a fusion protein in which a fragment of diphtheria toxin is fused to the cytokine interleukin 2 (IL-2) (Ontak) is approved for the treatment of cutaneous T-cell lymphoma ( 26 ). (asm.org)
  • MCL-1 becomes "primed" with prodeath proteins, such as BCL-2 homologous antagonist/killer (BAK), and inhibition with small molecular inhibitors, called BCL-2 homology domain-3 (BH3) mimetics, selectively kills the cancer cells. (sciencemag.org)
  • Recent studies showing preferences in binding between synthetic Bcl-2 homology domain 3 and antiapoptotic Bcl-2 family members in vitro have suggested that the antiapoptotic proteins Mcl-1 and Bcl-x L , but not Bcl-2, restrain proapoptotic Bak from inducing mitochondrial membrane permeabilization and apoptosis. (elsevier.com)
  • Recent studies showing preferences in binding between synthetic Bcl-2 homology domain 3 and antiapoptotic Bcl-2 family members in vitro have suggested that the antiapoptotic proteins Mcl-1 and Bcl-xL, but not Bcl-2, restrain proapoptotic Bak from inducing mitochondrial membrane permeabilization and apoptosis. (elsevier.com)
  • The intracellular signal transduction depends on the tyrosine kinase activity the ligand in the transmembrane β subunit triggers, permitting specific insulin receptor substrates (IRS-1 to −4) and Src-homology collagen (Shc) to phosphorylate, activating downstream mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways ( 6 ). (spandidos-publications.com)
  • Here, we report that the human Bcl-2 homology 3 (BH3)-only protein harakiri (Hrk) is a critical effector of 2-ME-induced JNK/mitochondria-dependent apoptosis in prostate cancer cells. (elsevier.com)
  • Antiapoptotic proteins include the multi-Bcl-2 homology (BH) domain proteins Bcl-2, Bcl-x L , Bcl-w, Mcl-1, Bcl-b, and Bcl2a1. (asm.org)
  • The protein encoded by this gene belongs to the BCL2 protein family. (wikipedia.org)
  • Gene Ontology (GO) annotations related to this gene include protein homodimerization activity and protein heterodimerization activity . (genecards.org)
  • Damage to the Bcl-2 gene has been identified as a cause of a number of cancers, including melanoma, breast, prostate, chronic lymphocytic leukemia, and lung cancer, and a possible cause of schizophrenia and autoimmunity. (wikipedia.org)
  • This fusion gene is deregulated, leading to the transcription of excessively high levels of Bcl-2. (wikipedia.org)
  • Therefore, the present study described the IGF1R gene and its associated signaling pathways, and offered details of IGF1R‑induced tumor chemoresistance associated with promoting cell proliferation, inhibition of apoptosis, regulation of ATP‑binding cassette transporter proteins and interactions with the extracellular matrix. (spandidos-publications.com)
  • The apoptosis was characterized by cell staining with Annexin V/FITC and propidium iodide and the apoptosis-associated gene expression profile was carried out using RT 2 Profiler PCR Array-Human Apoptosis. (biomedcentral.com)
  • Increased gene expression was observed for TNFRSF1B and Bid, associated with a reduction of Bcl-2, in individuals with P. vivax malaria. (biomedcentral.com)
  • Further in leukemia cell lines NB4 and HL-60, the protein level of target gene was measured by Western blot after overexpression miR-125b. (bvsalud.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)
  • Survivin is a new human gene encoding a structurally unique inhibitor of apoptosis proteins (IAP), apoptosis inhibitor, and plays an important role in the hyperplastic growth of tissues and tumors. (thefreedictionary.com)
  • BAK (Bcl-2 homologous antagonist/killer) is a novel pro-apoptotic gene of the Bcl-2 family. (biomedcentral.com)
  • The BAK gene encodes a 211-amino acid protein with a relative molecular weight ( M r) of 23,400. (biomedcentral.com)
  • Caspase-8 is a caspase protein, encoded by the CASP8 gene. (wikipedia.org)
  • A-kinase anchor protein 4 (AKAP4) gene and protein expression was monitored by quantitative polymerase chain reaction (qPCR), reverse transcription (RT)-PCR and Western blotting in normal colon tissue lysate, normal colon epithelial cells and in colon cancer cell lines viz. (biomedcentral.com)
  • Our studies showed that AKAP4 gene and protein expression was expressed in all colon cancer cells while no expression was detectable in normal colon cells. (biomedcentral.com)
  • 2. The composition of claim 1, wherein the modified eukaryotic cell further includes at least one rescue nucleic acid construct including an operon with an inducible promoter and encoding at least a portion of one or more of an exogenous histocompatibility antigen related gene, or a homologue thereof, or at least a portion of one or more superantigens. (patentsencyclopedia.com)
  • This protein localizes to mitochondria, and functions to induce apoptosis. (wikipedia.org)
  • BCL-2 is localized to the outer membrane of mitochondria, where it plays an important role in promoting cellular survival and inhibiting the actions of pro-apoptotic proteins. (wikipedia.org)
  • The rupture of the OMM that occurs during mitochondrial swelling can lead to the release of mitochondrial proapoptotic factors, such as cytochrome C ( 9 ), apoptosis-inducing factor (AIF) ( 10 ), second mitochondria-derived activator of caspases (SMAC)/direct IAP-binding protein with low PI (DIABLO) ( 11 ), and endonuclease G (EndoG) ( 12 ), and each of these factors can induce proapoptotic activity in different ways. (frontiersin.org)
  • The release of cytochrome c from mitochondria, which leads to activation of the intrinsic apoptotic pathway, is regulated by interactions of Bax and Bak with antiapoptotic Bcl-2 family members. (elsevier.com)
  • Together, our findings suggest that induction of the BH3-only protein Hrk is a critical step in 2-ME activation of the JNK-induced apoptotic pathway, targeting mitochondria by liberating proapoptotic protein Bak. (elsevier.com)
  • 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)
  • Inhibitor of apoptosis proteins IV: Intravenous NIH: National Institute PET: Positron emission tomography PR: Progesterone receptor SMAC: Second Mitochondria-derived Activator of Caspases SPECT: Single-photon emission tomography SUV: Standardized uptake values TGF-[beta]: Transforming growth factor-[beta] TNBC: Triple-negative breast cancer WHO: World Health Organization. (thefreedictionary.com)
  • however, in about 0.1-2% of electrons passing through the chain (this number derives from studies in isolated mitochondria, though the exact rate in live organisms is yet to be fully agreed upon), oxygen is instead prematurely and incompletely reduced to give the superoxide radical ( o ), most well documented for Complex I and Complex III . (popflock.com)
  • In response to pro-apoptotic signals (from pro-apoptotic proteins such as Bax), cytochrome c is released into the cell by the mitochondria, and they bind to a protein known as Apaf-1. (scientificamerican.com)
  • Thus, Hrk activation by 2-ME or its overexpression displaced Bak from the complex with antiapoptotic protein Bcl-x L , whereas deletion of the Hrk BH3 domain abolished its interaction with Bcl-x L , reducing the proapoptotic function of Hrk. (elsevier.com)
  • Overexpression of Bcl-2 1 and Fas-inhibitory molecules such as TOSO is the principle mechanism of apoptosis resistance in CLL cells. (intechopen.com)
  • Overexpression of Mcl-1 and Bcl-x L inhibited PE-induced MEF death. (asm.org)
  • Some evidence suggests that this may result from abnormal expression of Bcl-2 and increased expression of caspase-3. (wikipedia.org)
  • Next we found that ATO combined with CT induced cell apoptosis in Bel-7404 cells and upregulated the activation of apoptosis-related proteins cleaved-caspase-3, cleaved-caspase-9, and cleaved-poly(ADP-ribose) polymerase in a time-dependent manner. (biomedcentral.com)
  • Cytochrome c then forms a multi-protein complex known as the 'apoptosome' and initiates activation of the caspase cascade through caspase 9. (geneontology.org)
  • Hrk knockdown prevents 2-ME-mediated apoptosis by attenuating the decrease in mitochondrial membrane potential, subsequent cytochrome c (cyt c) release, and caspase activation. (elsevier.com)
  • During this process, caspase-2, caspase-8, caspase-9 and caspase-10 are involved in the initiation of apoptosis. (creative-diagnostics.com)
  • Further work revealed that caspase-8 was essential for the induction of the transcription factor "nuclear factor κB" ( NF-κB ) after stimulation through antigen receptors, Fc receptors, or Toll-like receptor 4 in T, B, and natural killer cells . (wikipedia.org)
  • For the death pathway, the caspase-8 zymogen is cleaved into subunits that assemble to form the mature, highly active caspase heterotetramer whereas for the activation pathway, the zymogen appears to remain intact perhaps to limit its proteolytic function but enhance its capability as an adapter protein. (wikipedia.org)
  • Several studies carried out to determine how protein toxins and immunotoxins containing these toxins kill target cells have reported caspase activation ( 13 , 16 , 17 , 30 , 33 ). (asm.org)
  • However, the steps leading up to caspase activation by these toxins that inhibit protein synthesis have not been elucidated. (asm.org)
  • Short peptides derived from the pro-apoptotic members of the Bcl-2 family can activate mechanisms that ultimately lead to cell death. (nih.gov)
  • The results show that Bax and Bak mediate non-redundant functions during MCMV infection and that the virus produces distinct inhibitors for each protein to counter the activity of these proteins. (nih.gov)
  • It remains to be determined if dual P2Y1/P2Y12 antagonists will be used in the clinic in place of the classical unimodal P2Y12 inhibitors. (ahajournals.org)
  • Following exposure to proteasome inhibitors, effective killing of human melanoma and myeloma cells, but not of normal proliferating melanocytes, was shown to involve p53-independent induction of the BH3-only protein NOXA. (aacrjournals.org)
  • As described herein, we discovered that proteasome inhibitors selectively induce the proapoptotic BH3-only protein NOXA in melanoma and myeloma cells, but not in normal melanocytes, providing new insight into the molecular basis for differential apoptotic responses of neoplastic versus normal cells. (aacrjournals.org)
  • 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)
  • Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. (rush.edu)
  • The two isoforms of Bcl-2, Isoform 1, and Isoform 2, exhibit a similar fold. (wikipedia.org)
  • Forms heterodimers with BCL2, E1B 19k protein, and BCL2L1 isoform Bcl-X(L). Interacts with myxoma virus protein M11L. (mybiosource.com)
  • A pro-apoptotic protein that is the short isoform of Bcl-X protein. (bvsalud.org)
  • Bcl-XL is an anti-apoptotic protein that is the long isoform of Bcl-X protein. (bvsalud.org)
  • Intact BH3 motif is required by BIK, BID, BAK, BAD and BAX for their pro-apoptotic activity and for their interaction with anti-apoptotic members of the Bcl-2 family. (abcam.cn)
  • The pro-apoptotic proteins in the BCL-2 family, including Bax and Bak, normally act on the mitochondrial membrane to promote permeabilization and release of cytochrome C and ROS, that are important signals in the apoptosis cascade. (wikipedia.org)
  • It belongs to the cytochrome c family of proteins. (wikipedia.org)
  • Cytochrome c is a highly conserved protein across the spectrum of species, found in plants, animals, and many unicellular organisms. (wikipedia.org)
  • All cytochrome c proteins contain a characteristic CXXCH (cysteine-any-any-cysteine-histidine) amino acid motif that binds heme. (wikipedia.org)
  • While most heme proteins are attached to the prosthetic group through iron ion ligation and tertiary interactions, the heme group of cytochrome c makes thioether bonds with two cysteine side chains of the protein. (wikipedia.org)
  • Upon release of cytochrome c to the cytoplasm, the protein binds apoptotic protease activating factor-1 (Apaf-1) . (wikipedia.org)
  • Cytochrome c can also catalyze several redox reactions such as hydroxylation and aromatic oxidation , and shows peroxidase activity by oxidation of various electron donors such as 2,2-azino- bis (3-ethylbenzthiazoline-6-sulphonic acid) ( ABTS ), 2-keto-4-thiomethyl butyric acid and 4-aminoantipyrine. (wikipedia.org)
  • Additionally, proteomic analysis found that the related proteins associated with apoptosis, oxidative stress, metabolism and membrane structure were affected. (bvsalud.org)
  • And metabolomic analysis verified that the related metabolic pathways, such as glycolysis, citrate cycle, oxidative phosphorylation, lipid and protein metabolism, were also significantly disrupted. (bvsalud.org)
  • Here we show that, after cell stress, p53 interacts with the pro-apoptotic mitochondrial membrane protein Bak. (nih.gov)
  • Bcl-XL localizes to the outer mitochondrial membrane and is overexpressed in most human NEOPLASMS. (bvsalud.org)
  • In summary, our results describe the involvement of HIV-1 PR in apoptosis, which is caused either by a direct effect of HIV-1 PR on mitochondrial membrane integrity or by its interaction with cellular protein BCA3. (biomedcentral.com)
  • Anti-apoptotic protein Bcl-2, which acts as a proto-oncogene, is a member of protective complexes that help to maintain the integrity of mitochondrial membrane. (biomedcentral.com)
  • The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. (bioon.com.cn)
  • Proteins were visualized using a goat anti-mouse secondary antibody conjugated to HRP and an ECL detection system. (acris-antibodies.com)
  • Mouse anti Human BAK antibody recognizes the Bcl-2 homologous antagonist/killer, also known as BAK, BCL2-like 7 protein, apoptosis regulator BAK, bcl2-L-7 or pro-apoptotic protein BAK. (bio-rad-antibodies.com)
  • Antibody response to the tumor-associated inhibitor of apoptosis protein survivin in cancer patients. (thefreedictionary.com)
  • Debiopharm has entered into a collaboration with Merck KGaA and Pfizer to evaluate Debio 1143, an oral, small molecule inhibitor of IAPs ( Inhibitor of Apoptosis Proteins ), in combination with avelumab, an investigational fully human anti-PD-L1 IgG1 monoclonal antibody, in advanced or metastatic Non-Small Cell Lung Cancer (NSCLC). (thefreedictionary.com)
  • Immunotoxins are a class of antitumor agents in which a powerful protein toxin is brought to the cancer cell by an antibody or an antibody fragment (for reviews, see references 28 , 29 , and 32 ). (asm.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)
  • MCMV-mediated inhibition of the pro-apoptotic Bak protein is required for optimal in vivo replication. (nih.gov)
  • The Bcl-2 family of proteins are the principle regulators of apoptosis, with two pro-apoptotic members, Bax and Bak, essential for apoptosis to proceed. (nih.gov)
  • These pro-apoptotic proteins are in turn activated by BH3-only proteins, and are inhibited by the function of BCL-2 and its relative BCL-Xl. (wikipedia.org)
  • The over-expression of the anti-apoptotic Bcl-2 protein in lymphocytes alone does not cause cancer. (wikipedia.org)
  • Other studies have shown that dendritic cell lifespan may be partly controlled by a timer dependent on anti-apoptotic Bcl-2. (wikipedia.org)
  • In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti-apoptotic action of BCL2 or its adenovirus homolog E1B 19k protein. (bioon.com.cn)
  • During the oncogenic transformation, some cancer cells become reliant on continuous expression of an anti-apoptotic protein, such as myeloid cell leukemia 1 (MCL-1). (sciencemag.org)
  • 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 induction of apoptosis. (umd.edu)
  • Tumors from ATO combined with CT-treated mice showed decreased levels of phosphorylated-STAT3 Tyr705 and the anti-apoptotic protein Bcl-2 but an increased level of pro-apoptotic protein Bax. (biomedcentral.com)
  • The results of the present study suggest that P. vivax infection induces apoptosis of CD4 + T cells mediated by two types of signaling: by activation of the TNFR1 death receptor (extrinsic pathway), which is amplified by Bid, and by decreased expression of the anti-apoptotic protein Bcl-2 (intrinsic pathway). (biomedcentral.com)
  • Although 2-ME has been shown to activate c-Jun-NH 2 -kinase (JNK) and mitochondrial-dependent apoptotic signaling pathways, the underlying mechanisms, including downstream effectors, remain unclear. (elsevier.com)
  • Many models for MOMP have been put forward, often involving pro‐apoptotic Bcl‐2 family members such as Bax and Bak. (embopress.org)
  • Furthermore, although various anti‐apoptotic Bcl‐2 family members inhibit cell death, they do not block mitochondrial fission or cristae rearrangements. (embopress.org)
  • Members of this family are cellular homologues that are either pro-apoptotic (Bax, Bik and Bid) or anti-apoptotic (Bcl-2 and Bcl-XL) [ 3 , 4 ]. (biomedcentral.com)
  • This protein is involved in the programmed cell death induced by Fas and various apoptotic stimuli. (wikipedia.org)
  • We found that BCA3 accelerates p53 transcriptional activity on the bax promoter, thus elevating the cellular level of pro-apoptotic Bax protein. (biomedcentral.com)
  • A pro-apoptotic protein and member of the Bcl-2 protein family that is regulated by PHOSPHORYLATION. (uchicago.edu)
  • Pro-apoptotic proteins, such as Bad and Bax, can bind to Bcl-2. (biomedcentral.com)
  • are pro-apoptotic proteins that trigger apoptosis when activated. (scientificamerican.com)
  • Montelukast also markedly decreased the phosphorylation of several proteins, such as with no lysine 1 (WNK1), protein kinase B (Akt), extracellular signal-regulated kinase 1/2 (Erk1/2), MAPK/Erk kinase (MEK), and proline-rich Akt substrate of 40-kDa (PRAS40), which might contribute to cell death. (mdpi.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)
  • Manicassamy S, Yin D, Zhang Z, Molinero LL, Alegre ML, Sun Z. A critical role for protein kinase C-theta-mediated T cell survival in cardiac allograft rejection. (uchicago.edu)
  • Recently, m41.1, a protein product encoded by the m41 open reading frame (ORF) of MCMV, has been shown to inhibit Bak activity in vitro. (nih.gov)
  • It is concluded that the VPA can inhibit proliferation of Jurkat cells which possibly associates with the decrease of BCL-2 expression. (bvsalud.org)
  • The present study was designed to test whether a grape seed polyphenolic extract (GSPE) previously shown to inhibit tau protein aggregation in vitro could benefit tau-mediated neuropathology and behavior deficits in JNPL3 transgenic mice expressing a human tau protein containing the P301L mutation. (isharonline.org)
  • B) HIV-1Ba-L exposure increases CD95/Fas apoptosis of T cells, which is inhibited by a TLR7/9 antagonist and anti-IFNα/β receptor blocking antibodies. (nih.gov)
  • Sensitivity to CD95/Fas-induced apoptosis shown for CD4+ T cells and CD8+ T cells from healthy donors following a 72 hour exposure to HIV-1Ba-L in the presence or absence of anti-IFNα/β receptor blocking antibodies or a TLR7/9 antagonist (n = 5). (nih.gov)
  • Our previous cohort study showed that cysteinyl leukotriene receptor antagonists, mainly montelukast, decreased the lung cancer risk in asthma patients. (mdpi.com)
  • The IGF-IGF1R axis consists of three receptor tyrosine kinases: IGF1R, insulin-like growth factor-2 receptor (IGF2R) and insulin receptor (INSR). (spandidos-publications.com)
  • Receptor-ligand systems of this group are critically involved in various cellular signalling pathways such as inflammation, lymphocyte homeostasis, apoptosis and tissue development [ 2 , 3 ]. (mdpi.com)
  • Furthermore, prostaglandin E2, a Galphas activating signal, was found to augment gamma ray-induced apoptosis, which was abolished by treatment with a prostanoid receptor antagonist. (bvsalud.org)
  • We concentrated on the most common classes of targeted therapies investigated in rhabdomyosarcoma to date, including those directed against receptor tyrosine kinases and associated downstream signaling pathways, the Hedgehog signaling pathway, apoptosis pathway, DNA damage response, cell-cycle regulators, oncogenic fusion proteins, and epigenetic modifiers. (aacrjournals.org)
  • This protein also interacts with the tumor suppressor P53 after exposure to cell stress. (wikipedia.org)
  • Recently, the function of IGF1R in chemotherapeutic resistance has gained increasing attention, and relevant mechanisms of inducing resistance in cancer cells include overexpressing multi-drug-resistant proteins, dysregulating cell survival and death and interacting with the tumor microenvironment ( 7 ). (spandidos-publications.com)
  • 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)
  • Both pharmacological factors, including inadequate drug concentration at the tumor site, and cellular factors can contribute to clinical resistance [ 2 ]. (biomedcentral.com)
  • 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)
  • In this review, we describe the role of the Epstein-Barr virus in gastric carcinogenesis, summarizing the functions of the Epstein-Barr virus-encoded viral proteins and related epigenetic alterations as well as the roles of Epstein-Barr virus-encoded and virally modulated cellular miRNAs. (hindawi.com)
  • Here, we report the first NMR solution structure of a photoswitchable peptide derived from the proapoptotic protein Bak in complex with the antiapoptotic protein Bcl-x(L). This structure provides insight into the molecular mechanism, by which the increased affinity of such photopeptides compared to their native forms is achieved, and offers a rationale for the large differences in the binding affinities between the helical and nonhelical states. (nih.gov)
  • The multidomain proapoptotic protein BAK, but not its orthologue BAX, was found to be essential for bortezomib-induced apoptosis in MPM cell lines. (le.ac.uk)
  • Involvement of the proapoptotic protein Bak in this process suggested the possible interaction between Hrk and Bak. (elsevier.com)
  • Paul T has suggested it may be possible to add in (manually) any homologous genes that may have diverged too much to be recognized by the existing PANTHER HMMs. (geneontology.org)
  • Moderate ER stress induced the expression of key unfolded protein response genes, BiP, CHOP, and XBP1s to significantly higher levels in B7-H4 transgenic islets compared with wild type. (ubc.ca)
  • The Bcl-2 family of genes appears to be important in the regulation of apoptosis. (biomedcentral.com)
  • The expression of the cell death-inducing protein, Bak, was investigated in 41 cases of Hodgkin's disease and was correlated with Epstein-Barr virus (EBV) status. (nih.gov)
  • Bcl-2 expression is frequent in small cell lung cancer, accounting for 76% cases in one study. (wikipedia.org)
  • However, mammosphere forming assay indicated that ATF3 overexpressed colon cancer cells form larger and more budding sites compared to control, which is associated with an increase of cluster of differentiation 44 (CD44) expression and a decrease of retinoblastoma (Rb) and tight junction protein zonula occludens (ZO)-1. (umd.edu)
  • The expression of Bcl-2 family proteins, ERK and Akt signaling pathways were examined by Western blot analysis. (biomedcentral.com)
  • Furthermore, the expression of Bim was increased instead of Bax and Bcl-2. (biomedcentral.com)
  • In human non-Hodgkin lymphomas, high expression of Bcl-2 but not Bcl-xL predicted sensitivity to ABT-263. (edu.au)
  • When expressed in HeLa cells, F1L blocked apoptosis induced by forced expression of the BH3-only proteins, Bim, Puma and Noxa. (edu.au)
  • GalphasQL up-regulated the Bak expression at the levels of protein and mRNA. (bvsalud.org)
  • Expression of GalphasQL increased basal and gamma ray-induced luciferase activity of cAMP response element binding protein (CREB) and AP-1, and the binding of CREB and AP-1 to Bak promoter. (bvsalud.org)
  • Together, our findings demonstrate that over-expression of B7-H4 amplifies β-cell glucose-stimulated Ca²+ responses and the unfolded protein response during ER stress, revealing novel roles for B7-H4 in the pancreatic β-cell. (ubc.ca)
  • The protein expression of UGT1A1, 1A6 and 2B were decreased in acute liver injury rats. (bvsalud.org)
  • Increased sensitivity of Caco-2 cells to ABT-737 after addition of SU9516 correlated well with SU9516-induced decrease of Mcl-1 expression while we have not observed downregulation of Mcl-1 after the treatment of HT29 cells with SU9516. (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)
  • DZNep represses Bcl-2 expression and modulates apoptosis sensitivity in response to Nutlin-3a. (rush.edu)
  • The expression of HKII in MSCs exposed to H 2 O 2 was evaluated, and HKII-targeting miRNA was screened based on miRNA-target prediction databases. (conicyt.cl)
  • The effect of H 2 O 2 on the expression of the selected HKII-targeting miRNA was examined and the effect of modulation of the selected HKII-targeting miRNA using anti-miRNA on H 2 O 2 -induced apoptosis of MSC was evaluated. (conicyt.cl)
  • H 2 O 2 (600 μΜ ) induced cell death of MSCs and decreased mitochondrial HKII expression. (conicyt.cl)
  • We have identified miR-181a as a HKII-targeting miRNA and H 2 O 2 increased the expression of miR-181a in MSCs. (conicyt.cl)
  • Inhibition of NF-kappaB-dependent Bcl-xL expression by clusterin promotes albumin-induced tubular cell apoptosis. (uchicago.edu)
  • Interaction between unfold protein response (UPR) and autophagy may play an important role to maintain the muscle protein quality control. (ajkinesiol.org)
  • Although both drugs avidly bind Bcl-2, Bcl-xL, and Bcl-w in vitro, we find that Bcl-2 is the critical target in vivo, suggesting that patients with tumors overexpressing Bcl-2 will probably benefit. (edu.au)
  • Similarly, to initiator caspases, GB activates the proapoptotic Bcl-2 member BID to switch on the intrinsic mitochondrial death pathway [ 34 - 37 ]. (hindawi.com)
  • Once formed, the apoptosome goes on to activate a group of proteins known as caspases. (scientificamerican.com)
  • Earlier, we found that grape seed extract (GSE) increases Cip/p21 protein level and inhibits growth and induces apoptosis in human colon carcinoma HT29 cells both in vitro and in vivo. (isharonline.org)
  • Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN. (uchicago.edu)
  • Petrella A, Ercolino SF, Festa M, Gentilella A, Tosco A, Conzen SD, Parente L. Dexamethasone inhibits TRAIL-induced apoptosis of thyroid cancer cells via Bcl-xL induction. (uchicago.edu)
  • Cytotoxic T lymphocytes (CTL) and natural killer (NK) cells are essential to the host defense against pathogen-infected or transformed cells [ 1 - 6 ]. (hindawi.com)
  • Two major isoforms of the protein exist due to ALTERNATIVE SPLICING of the BCL2L1 mRNA and are referred to as Bcl-XS and Bcl-XL. (bvsalud.org)
  • A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. (harvard.edu)
  • The Bcl-2 family of proteins includes the major regulators and effectors of the intrinsic apoptosis pathway. (nih.gov)
  • The key factor in protein synthesis pathway for protein quality control is mammalian target of rapamycin complex 1 (mTORC1), indeed aging impairs contraction-induced human skeletal muscle mTORC1 signaling and protein synthesis. (ajkinesiol.org)
  • Mcl-1, but not Bcl-x L , was rapidly degraded after PE treatment, consistent with a role for Mcl-1 in the PE death pathway. (asm.org)
  • Bcl-2 family members are essential regulators of the mitochondrial (intrinsic) apoptosis pathway ( 1 , 21 ). (asm.org)
  • bcl-2-Associated X Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • Proto-Oncogene Proteins c-bcl-2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (rush.edu)
  • The ligand-binding specificity determinant is reflected in the amino-terminal cysteine-rich domain of the extracellular α subunit, primarily recognizing and binding to IGF-1 and IGF-2. (spandidos-publications.com)
  • A member of the bcl-2 protein family that plays a role in the regulation of APOPTOSIS and is a regulatory subunit for PROTEIN PHOSPHATASE 1. (bvsalud.org)
  • Induction of NOXA at the protein level was preceded by enhanced transcription of NOXA mRNA. (aacrjournals.org)
  • The m38.5 protein encoded by murine CMV (MCMV) has been identified as Bax-specific inhibitor of apoptosis. (nih.gov)
  • Finally, Hrk is also involved in the 2-ME-mediated reduction of X-linked inhibitor of apoptosis through Bak activation in prostate cancer cells. (elsevier.com)
  • Physiologically based pharmacokinetic and pharmacodynamic modeling of an antagonist (SM-406/AT-406) of multiple inhibitor of apoptosis proteins (IAPs) in a mouse xenograft model of human breast cancer," Biopharmaceutics & Drug Disposition, vol. (thefreedictionary.com)
  • The inhibitor of apoptosis protein family and its antagonists in acute leukemias. (thefreedictionary.com)
  • ASGQGPGPPRQE-C , corresponding to N terminal amino acids 2-13 of Human Bak(Peptide available as ab22900 . (abcam.com)
  • Antibodies to Bcl-2 can be used with immunohistochemistry to identify cells containing the antigen. (wikipedia.org)
  • Search, Find and Buy Antibodies, ELISA Kits and Proteins. (antibodies-online.com)
  • p>When browsing through different UniProt proteins, you can use the 'basket' to save them, so that you can back to find or analyse them later. (uniprot.org)
  • However, results in the ability of these isoforms to bind to the BAD and BAK proteins, as well as in the structural topology and electrostatic potential of the binding groove, suggest differences in antiapoptotic activity for the two isoforms. (wikipedia.org)
  • isoforms]] of the protein. (wikidoc.org)
  • Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein. (harvard.edu)
  • The tumour suppressor activity of the p53 protein has been explained by its ability to induce apoptosis in response to a variety of cellular stresses. (nih.gov)
  • The primary regulators of apoptosis are proteins belonging to a group known as the Bcl-2 family. (scientificamerican.com)
  • SCIENTIFIC COMMUNIQUÉ I provided an outline of the various physiological modifications taking place on proteins and the clinical relevance to our technology programs. (clinuvel.com)
  • Hrk mRNA and protein are preferentially upregulated by 2-ME, and Hrk induction is dependent on the JNK activation of c-Jun. (elsevier.com)
  • Interestingly, pancreatic β-cells also express high levels of B7-H4 mRNA and moderate levels of B7-H4 protein. (ubc.ca)
  • Efficacy evaluation of ATO combined with CT on xenograft was carried in nude mice and related proteins were analysis by Immunohistochemistry assays. (biomedcentral.com)
  • Bcl-2, bak, p53, Ki67 and latent membrane protein-1 (LMP1) were detected by immunohistochemistry in pre-treatment lymph node biopsies. (bvsalud.org)
  • These proteases are essential for viral polyprotein processing and also cleave cellular proteins. (asm.org)
  • Stimulatory heterotrimeric GTP-binding proteins (Gs protein) stimulate cAMP generation in response to various signals, and modulate various cellular phenomena such as proliferation and apoptosis. (bvsalud.org)
  • In response to cellular stress such as DNA damage, the p53 protein becomes stabilized. (embopress.org)
  • A novel biologically based treatment approach uses agents targeting the proteasome, a universal and broadly active cellular complex responsible for regulating protein degradation and maintenance of normal cell function ( 1 , 2 ). (aacrjournals.org)
  • The cellular response to ER stress is well known as unfold protein response (UPR) which seeks to recover ER function. (ajkinesiol.org)
  • Cell apoptosis induced by ATO combined with CT was detected by Annexin V/PI staining and apoptosis-related proteins were detected by western blotting. (biomedcentral.com)
  • As substrates for the proteasome include regulatory proteins involved in cell cycle progression, apoptosis, and angiogenesis, targeting the proteasome represents an attractive therapeutic approach for cancer treatment ( 3 ). (aacrjournals.org)
  • The transformation of gastrointestinal epithelial tissue to carcinomas has been shown to be associated with the progressive inhibition of apoptosis [ 1 , 2 ]. (biomedcentral.com)