Killer Factors, Yeast: Protein factors released from one species of YEAST that are selectively toxic to another species of yeast.bcl-2 Homologous Antagonist-Killer Protein: 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.Mycotoxins: Toxic compounds produced by FUNGI.Killer Cells, Natural: 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.Whale, Killer: 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.Killer Cells, Lymphokine-Activated: 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.Hormone Antagonists: 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.Natural Killer T-Cells: 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.Dopamine Antagonists: 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.Cytotoxicity, Immunologic: 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.Excitatory Amino Acid Antagonists: Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.Neurokinin-1 Receptor Antagonists: Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.Narcotic Antagonists: Agents inhibiting the effect of narcotics on the central nervous system.Histamine H2 Antagonists: 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.Interleukin 1 Receptor Antagonist Protein: 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.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Muscarinic Antagonists: 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, Natural Killer Cell: 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.Leukotriene Antagonists: A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.Receptors, Leukotriene: 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.Carcinoma, Lewis Lung: 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.QuinolinesAcetates: Derivatives of ACETIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxymethane structure.Anti-Asthmatic Agents: Drugs that are used to treat asthma.Lung Neoplasms: Tumors or cancer of the LUNG.Genes, bcl-2: 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.Antibodies: 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).bcl-2-Associated X Protein: 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.Molecular Sequence Data: 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.Proto-Oncogene Proteins c-bcl-2: 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.Antibody Specificity: 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.Amino Acid Sequence: 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.Cyclic AMP Response Element-Binding Protein: 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.Colonic Neoplasms: Tumors or cancer of the COLON.HCT116 Cells: Human COLORECTAL CARCINOMA cell line.Cell Line, Tumor: A cell line derived from cultured tumor cells.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Apoptosis: 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.Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.bcl-X Protein: A member of the bcl-2 protein family that plays a role in the regulation of APOPTOSIS. 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.Endoplasmic Reticulum: A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)Caspases: A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.Mitochondria: Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)Leukemia, Lymphocytic, Chronic, B-Cell: A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.Phloroglucinol: A trinitrobenzene derivative with antispasmodic properties that is used primarily as a laboratory reagent.PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Myeloid Cell Leukemia Sequence 1 Protein: A member of the myeloid leukemia factor (MLF) protein family with multiple alternatively spliced transcript variants encoding different protein isoforms. In hematopoietic cells, it is located mainly in the nucleus, and in non-hematopoietic cells, primarily in the cytoplasm with a punctate nuclear localization. MLF1 plays a role in cell cycle differentiation.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Bicyclo CompoundsRespiratory System Abnormalities: Congenital structural abnormalities of the respiratory system.Jurkat Cells: A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.Antigens, CD95: A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.Cell Line: Established cell cultures that have the potential to propagate indefinitely.T-Lymphocytes: Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.

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)

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/
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 ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
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 ...
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. 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 ...
Diş həkimi Fərid Zeynalov. Dental Expert stomatoloji klinika, Bakı Azərbaycan, Avrasiya Hospital, Dental One, Pulpa Dent, MediStyle, InterMed
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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 ...
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 ...
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 ...
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. ...
Gold Label Bak Foong Pills (Bai Feng Wan) is a traditional chinese remedy to regulate & relieve monthly discomforts, and nourishment after childbirth. Shop Now!
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To navigate through the Ribbon, use standard browser navigation keys. To skip between groups, use Ctrl+LEFT or Ctrl+RIGHT. To jump to the first Ribbon tab use Ctrl+[. To jump to the last selected command use Ctrl+]. To activate a command, use Enter. ...
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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 ...
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 ...
Bitkisel ve Hayvansal Yetiştiricilik, Hastalıkları, Zararlıları, Besin Noksanlıkları, Kanunları, Desteklemeleri, Mutfakta ve Sanayide kullanımı, Tarım marketi, Tarım Market
Bitkisel ve Hayvansal Yetiştiricilik, Hastalıkları, Zararlıları, Besin Noksanlıkları, Kanunları, Desteklemeleri, Mutfakta ve Sanayide kullanımı, Tarım marketi, Tarım Market
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 ...
We have identified a new pro-apoptotic Bcl-2-related protein Bok, based on its binding to an ovarian anti-apoptosis protein Mcl-1. In addition to its restricted expression in several reproductive tissues, Bok also shows a selective heterodimerization property by interacting with some (Mcl-1, BHRF1, and Bfl-1) but not other (Bcl-2, Bcl-xL, and Bcl-w) anti-apoptotic proteins. Coupled with findings showing that Bok-induced apoptosis could only be antagonized by selective anti-apoptotic proteins, the present data suggest that different pro- and anti-apoptotic Bcl-2 protein pairs may play tissue-specific roles in the regulation of apoptosis. Because of the restricted expression of Bok to ovarian granulosa cells and several reproductive tissues characterized by hormonally regulated cyclic cell turnover, further analyses of Bok action in the gonads and uterus could provide unique models to study the hormonal regulation of apoptosis. Because most of the Bcl-2-related proteins have been identified in the ...
Our lab is cross-disciplinary, bringing together computational biology, protein design, and molecular biology approaches. We assess the structural bioinformatics of OMPs (outer membrane proteins) and apply the results to de novo OMP protein design and to native OMP manipulation.. OMPs are a ripe target for cancer therapeutics. Mitochondria have recently become a focus of cancer therapies due to the fact that mitochondrial outer membrane permeabilization leads to apoptosis or necrosis. We explore mitochondrial membrane permeabilization through manipulation of the OMP pores that already exist in the mitochondrial outer membrane. This may have pharmaceutical consequences because tumorigenic mitochondrial membranes can be selectively targeted in themselves as they have been shown to accumulate lipophilic cations.. Beyond this mechanistic understanding, knowledge of the relationship between OMP chemistry and structure will allow new OMPs to be designed for use in vaccines and will facilitate ...
Apoptosis resistance is the major cause of chemotherapy failure in most kinds of cancers, including Burkitt lymphomas (BL). To elucidate molecular mechanisms regulating the development of apoptosis resistance, a panel of 15 BL cell lines was investigated for apoptosis induction upon treatment with microtubule inhibitors taxol, nocodazole and vincristine. Significant differences were observed in the extent of apoptosis induction among BL cell lines examined. Interestingly, cell lines exhibiting resistance to taxol- or nocodazole-induced apoptosis, showed development of polyploidy (,4N) and vice versa, displaying an inverse relationship between apoptosis and polyploidy induction. Further, in sensitive cell lines taxol-induced apoptosis was accompanied by caspase activation, Bid cleavage and Mcl-1 down-regulation. In contrast, most apoptosis resistant cell lines exhibited a loss of Bax and Bak expression and showed prolonged mitotic arrest with ,4N DNA content upon treatment. To gain mechanistic ...
Apoptosis is the physiological process used by an organism to selectively eliminate cells that are no longer needed, have been damaged or are dangerous ( Kerr et al., 1972). This process, critical for sculpting organs during development and ensuring homeostasis throughout life, has been conserved during evolution ( Vaux and Strasser, 1996). Defects in the control of apoptosis have been implicated as a cause or a contributing factor in a variety of diseases. For example, abnormal survival of cells that should be killed can cause cancer ( Strasser et al., 1990) or autoimmune disease ( Bouillet et al., 1999; Strasser et al., 1991b; Watanabe-Fukunaga et al., 1992), whereas premature death of normally long-lived cells may be the cause of certain degenerative disorders ( Barr and Tomei, 1994).. Genetic and biochemical studies have identified two major pathways to programmed cell death that are largely independent ( Strasser et al., 1995). On the one hand, apoptosis can be triggered by ligation of a ...
Deficient expression of Bak in a clonal Jurkat cell line. (A) Wild-type or the variant Jurkat cell line, Bak−, were incubated in 1% NP-40 lysis buffer for 30
Most overseas Chinese, especially those living in South East Asia, have tried Bak Kut Teh. Its the type of food that people either love or hate, but one thing for sure is that they will never forget it. Bak Kut Teh (Bah Kut Teh) or Rou Ku Cha in...
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Web sitesi ile ilgili bir sorunu bildirmek için, [email protected] adresine e-posta gönderin. Diğer iletişim bilgileri için Debian iletişim sayfasına bakın.. İçerik Telif Hakkı © 1997 - 2018 SPI Inc.; Lisans koşullarına bakın. Debian bir https://www.debian.org/trademark tescilli markasıdır Bu site hakkında daha fazlasını öğrenin.. ...
Incredibly, Bok, who is president emeritus of Harvard University, manages to come off here as a Milquetoast, even though he is addressing controversial questions and providing intelligent commentary.
Bastide Le Petit Clos, Perpignan: Tarafsız yorumları okuyun, gerçek gezgin fotoğraflarına bakın. TripAdvisorın interaktif haritasını kullanarak konuma ve yakındaki restoran ve gezilecek yer seçeneklerine göz atın. Konaklamanız için fiyatları karşılaştırın ve en iyi teklifi alın.
以前我一直在買專櫃的衣服,認為要現場挑衣服才有保障,不太敢在網路上買衣服,因為害怕收到貨時與圖色差太大,或是怕…
TY - JOUR. T1 - Intramitochondrial recruitment of endolysosomes mediates Smac degradation and constitutes a novel intrinsic apoptosis antagonizing function of XIAP E3 ligase. AU - Hamacher-Brady, Anne. AU - Choe, S. C.. AU - Krijnse-Locker, J.. AU - Brady, Nathan Ryan. PY - 2014/12/1. Y1 - 2014/12/1. N2 - Intrinsic apoptosis involves BH3-only protein activation of Bax/Bak-mediated mitochondrial outer membrane permeabilization (MOMP). Consequently, cytochrome c is released from the mitochondria to activate caspases, and Smac (second mitochondria-derived activator of caspases) to inhibit XIAP-mediated caspase suppression. Dysfunctional mitochondria can be targeted for lysosomal degradation via autophagy (mitophagy), or directly through mitochondria-derived vesicle transport. However, the extent of autophagy and lysosomal interactions with apoptotic mitochondria remains largely unknown. We describe here a novel pathway of endolysosomal processing of mitochondria, activated in response to canonical ...
Bak1 - mouse gene knockout kit via CRISPR, 1 kit. |dl||dt|Kit Component:|/dt||dd|- |strong|KN301970G1|/strong|, Bak1 gRNA vector 1 in |a href=http://www.origene.com/CRISPR-CAS9/Detail.
Et par søte joggebukser fra Fixoni. Disse joggebuksene har god tøystrikk i anklene og midjen, og de har lomme foran og bak. Midjen kan brettes ned. |br||br|Midje: 100 % bomull. Oeko-Tex Standard 100-sertifisert. |br|Vask: maskin 40 grader. |br||br|Farge: lilla, grå.
Mantle cell lymphoma (MCL) is characterized by a profound deregulation of the mechanisms controlling cell-cycle progression and survival. We herein show that the combination of 9-cis-retinoic acid (RA) and IFN-α induces marked antiproliferative and proapoptotic effects in MCL cells through the modulation of critical targets. Particularly, IFN-α enhances RA-mediated G0-G1 cell accumulation by downregulating cyclin D1 and increasing p27Kip1 and p21WAF1/Cip1 protein levels. Furthermore, RA/IFN-α combination also induces apoptosis by triggering both caspases-8 and -9 resulting in Bax and Bak activation. In particular, RA/IFN-α treatment downregulates the antiapoptotic Bcl-xL and Bfl-1 proteins and upregulates the proapoptotic BH3-only Noxa protein. Sequestration of Mcl-1 and Bfl-1 by upregulated Noxa results in the activation of Bid, and the consequent induction of apoptosis is inhibited by Noxa silencing. Noxa upregulation is associated with nuclear translocation of the FOXO3a transcription ...
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Bok choy is a staple of many Asian dishes and particularly of Chinese food, where its a common element of many stir-fry dishes. Its a member of...
Cabañas El Rocio, Colon: Tarafsız yorumları okuyun, gerçek gezgin fotoğraflarına bakın. TripAdvisorın interaktif haritasını kullanarak konuma ve yakındaki restoran ve gezilecek yer seçeneklerine göz atın. Konaklamanız için fiyatları karşılaştırın ve en iyi teklifi alın.
When cells kill themselves, they usually do so by activating mechanisms that have evolved specifically for that purpose. These mechanisms, which are broadly conserved throughout the metazoa, involve two processes: activation in the cytosol of latent cysteine proteases (termed caspases), and disruption of mitochondrial functions. These processes are linked in a number of different ways. While active caspases can cleave proteins in the mitochondrial outer membrane, and cleave and thereby activate certain pro-apoptotic members of the Bcl-2 family, proteins released from the mitochondria can trigger caspase activation and antagonise IAP family proteins. This review will focus on the pro-apoptotic molecules that are released from the mitochondria of cells endeavouring to kill themselves. This article is part of a Special Issue entitled Mitochondria: the deadly organelle ...
Commentary 2801 Introduction Apoptosis is essential for normal development and tissue homeostasis, and perturbations in its regulation contribute to numerous pathological conditions, including cancer and autoimmune and degenerative diseases (Adams and Cory, 2007; Meier and Vousden, 2007). There are two main pathways that lead to apoptosis: the extrinsic pathway, which is triggered following the activation of cell-surface-expressed death receptors such as CD95 (also known as Fas receptor) and tumour necrosis factor receptor; and the intrinsic pathway, which is activated by cellular stress and is regulated primarily at the level of mitochondria by the Bcl-2 family of proteins (Fig. 1). The intrinsic apoptotic pathway is initiated in response to a variety of stress signals (Willis and Adams, 2005), and a complex interplay of Bcl-2 proteins relays this signal to the mitochondrial outer membrane (OM) to initiate Bak and Bax activation, oligomerisation and OM damage (Fig. 1). Breaching the ...
I sowed Wong Bok seeds in March, April and May (autumn). Germination was near 100% and grow very fast. So I thought that it was a suitable time to grow wong bok. After 3 months our wong bok did not show any sign of leaves developing firm compact head but the leaves were lying flat towards the ground. We even tie the leaves together to make it shape like a barrel. All of them bolted. We have about 5 plants left growing in the patch which has not flower yet but I reckon it will bolt too.. ...
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På Veritabel.no er det saken som ligger til grunn for den gode debatten. Det vil på ingen måte aksepteres at personer tar fokus fra saken. Hvem som står bak kommentaren er likegyldig, så lenge det føres en saklig debatt. Derfor kan du være anonym hvis ønskelig.. ...
Ziphood fra Wax med klassisk snøring, brodering og stort trykk på forsiden, trykk bak. Materiale: 80% Bomull, 20% Polyester. Modellen er 182cm og avbildet i M.
IJIASR fen bilimlerinde güncel sorunlar üzerine yenilikçi bakış açısı getiren çalışmalara öncelik vermekle birlikte, aşağıdaki alanlarda yer alan bilimsel çalışmaları kabul etmektedir.. ...
Developing novel chemo-prevention techniques and advancing treatment are key elements to beating lung cancer, the most common cause of cancer mortality worldwide. Our previous cohort study showed that cysteinyl leukotriene receptor antagonists, mainly montelukast, decreased the lung cancer risk in asthma patients. In the current study, we conducted in vivo and in vitro experiments to demonstrate the inhibiting effect of montelukast on lung cancer and to investigate the underlying mechanisms. Using Lewis lung carcinoma-bearing mice, we showed that feeding montelukast significantly delayed the tumor growth in mice (p < 0.0001). Montelukast inhibited cell proliferation and colony formation and induced the cell death of lung cancer cells. 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. Montelukast also markedly
A-371191 is a novel Bcl-XL antagonist. Bcl-XL is one of the anti-apoptotic Bcl-2 family members that plays a key role in the regulation of apoptosis. Overexpression of Bcl-XL occurs in numerous cancers and its overexpression correlates with increased resistance to many chemocytotoxic drugs.
ok so here goes this is my first blog ever and i have a big secret ok so i was sitting on the couch last nite and my cousins boyfriend had lit up a joint and we started smoking and he had always told me he wanted to fuck me but i said no b/c he went out with my cousin and he stole my hat and i said u cant do that and he said yes i can and i took it bak and he leand in to my face and by that time i was so high i didnt know what i was doing and i said u kno u want to kiss me and he said no u want to kiss me and i said no u want to kiss me and i said if u want to kiss me why dont u go for it which was a big mistake b/c he kissed me and i kissed him bak in my heart i knew it was wrong but it felt so right that i couldnt stop and we got done kissing and we sat bak and watched a little more of Tila Tequla and he kissed me again and we couldnt stop kissing but by this time everyone else was alseep and we didnt stop kissing and we moved to the bed kissing and the next thing i know is we are ...
ok so here goes this is my first blog ever and i have a big secret ok so i was sitting on the couch last nite and my cousins boyfriend had lit up a joint and we started smoking and he had always told me he wanted to fuck me but i said no b/c he went out with my cousin and he stole my hat and i said u cant do that and he said yes i can and i took it bak and he leand in to my face and by that time i was so high i didnt know what i was doing and i said u kno u want to kiss me and he said no u want to kiss me and i said no u want to kiss me and i said if u want to kiss me why dont u go for it which was a big mistake b/c he kissed me and i kissed him bak in my heart i knew it was wrong but it felt so right that i couldnt stop and we got done kissing and we sat bak and watched a little more of Tila Tequla and he kissed me again and we couldnt stop kissing but by this time everyone else was alseep and we didnt stop kissing and we moved to the bed kissing and the next thing i know is we are ...
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BAK1 belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic regulators that are…
Venetoclax (ABT-199, GDC-0199)是一种Bcl-2选择性抑制剂,无细胞试验中Ki为<0.01 nM,比作用于Bcl-xL和Bcl-w选择性高4800倍以上,对Mcl-1没有抑制活性。有研究证明 Venetoclax 在三阴性乳腺癌 MDA-MB-231 细胞中诱导细胞生长抑制,凋亡,细胞周期停滞和自噬。Phase 3。
These pro-apoptotic proteins are in turn activated by BH3-only proteins, and are inhibited by the function of BCL-2 and its ... This is the first FDA approval of a protein-protein inhibitor of BCL-2. Bcl-2 has been shown to interact with: BAK1, BCAP31, ... Tagami S, Eguchi Y, Kinoshita M, Takeda M, Tsujimoto Y (Nov 2000). "A novel protein, RTN-XS, interacts with both Bcl-XL and Bcl ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". The ...
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 (Feb 2014). "Building blocks of the apoptotic pore ... 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-x protein MeSH D12.644.360.075.718.968 --- bh3 interacting domain death agonist protein MeSH D12.644.360.100 --- ca(2+)- ... 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 --- ... x-linked inhibitor of apoptosis protein MeSH D12.644.360.075.718 --- proto-oncogene proteins c-bcl-2 MeSH D12.644.360.075. ...
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: 6075-6084. doi:10.1021/bi060142r. ...
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 ...
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 ... The apoptosomes bind to and activate caspase-9, another free-floating protein. The caspase-9 then cleaves the proteins of the ... causing oxidized protein levels to increase. This led researchers to conclude that oxidation of cellular proteins is ...
... 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 ...
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 ...
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 ...
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 ...
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 ...
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]. ...
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 (Feb 2014). "Building blocks of the apoptotic pore ... 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 ...
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- ...
... 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 ...
Membrane Proteins/metabolism*. *Proto-Oncogene Proteins c-bcl-2/metabolism*. *Serine Endopeptidases/metabolism* ... We report here that the Bcl-2 proapoptotic family member, Bak, plays a dominant role in GrB-mediated mitochondrial apoptotic ... We report here that the Bcl-2 proapoptotic family member, Bak, plays a dominant role in GrB-mediated mitochondrial apoptotic ... Bak-deficient mitochondria did not release cytochrome c in response to GrB-treated cytosol unless recombinant Bak protein was ...
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. ...
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 ( ...
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 ...
These pro-apoptotic proteins are in turn activated by BH3-only proteins, and are inhibited by the function of BCL-2 and its ... This is the first FDA approval of a protein-protein inhibitor of BCL-2. Bcl-2 has been shown to interact with: BAK1, BCAP31, ... Tagami S, Eguchi Y, Kinoshita M, Takeda M, Tsujimoto Y (Nov 2000). "A novel protein, RTN-XS, interacts with both Bcl-XL and Bcl ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". 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 ...
... and BCL2-homologous antagonist/killer (BAK), 2 proapoptotic BCL-2 family proteins that together represent an essential gateway ... Loss of pancreatic IKK? causes defective autophagic protein degradation, leading to accumulation of p62-mediated protein ... LDL receptor-related protein (LRP1) is an endocytic and cell-signaling receptor that regulates cell migration. In this study, ... To directly investigate this idea, we tested whether tissue-specific deletion in the mouse CNS of BCL2-associated X protein ( ...
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 ...
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. ...
... 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 ...
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 ...
... of proteins, those which are pro-apoptotic and anti-apoptotic. Bcl-2 is pro-cell death and, for instance, Bak (Bcl-2 homologous ... antagonist killer), Bax (Bcl-2 Associated X), and Bid (Bh3-interacting domain) proteins are expressed to inhibit apoptosis. ... The p53 protein is one of the most widely studied tumour suppressor proteins in cancer research. For the sake of this ... Here we focus on specific proteins expressed by the skin following exposure to UV radiation and which play a part in the damage ...
... a protein forming part of a mitochondrial pore complex that stands as a receptor for the proapoptotic protein, Bcl-2-associated ... The major component of RISC is the Argonaute (Ago) protein. In mammalian cells there are four Ago proteins which are all ... also demonstrated that EBV BHRF1 miRNAs can promote cell survival by interacting with several proapoptotic proteins such as Bcl ... might promote cell transformation by activating antiapoptotic protein Bcl-2 [94]. In addition to these effects, EBV infection ...
... only protein [[BH3 interacting domain death agonist,Bid]] into its truncated form, tBid. BH-3 only members of the Bcl-2 family ... an antagonist of inhibitors of apoptosis proteins ([[Inhibitor of apoptosis,IAPs]]). Soluble FasL is less active than its ... Interactions == Fas ligand has been shown to [[Protein-protein interaction,interact]] with: {{div col,colwidth=20em}} * [[ ... Bcl-xL), allowing [[Bcl-2 homologous antagonist killer,Bak]] and [[Bcl-2-associated X protein,Bax]] to translocate to the outer ...
  • The interest in this unusual mitochondrial state increased exponentially in the 1990s after the MPT was shown to be a strategic regulator of cell death ( 2 ). (frontiersin.org)
  • Under normal physiological conditions, the p53 protein is maintained at low intracellular levels by its negative regulator, the E3 ubiquitin ligase Mdm2, which targets p53 for ubiquitin‐dependent degradation through the proteasome [ 2 ]. (embopress.org)
  • 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)
  • A computational model, validated in vivo, indicated that high BCL-xL expression confers resistance to MCL1 repression, thereby identifying a patient-selection strategy for the clinical development of MCL1 inhibitors. (nih.gov)
  • Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. (rush.edu)
  • 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)
  • 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)
  • 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)
  • E-G. Gene expression repression by triptolide at 2 hours (E), 4 hours (F) and 6 hours (G). The genes were ranked by the extent of repression. (nih.gov)
  • Caspase-8 is a caspase protein, encoded by the CASP8 gene. (wikipedia.org)
  • 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). (cdc.gov)
  • The BAK gene encodes a 211-amino acid protein with a relative molecular weight ( M r) of 23,400. (biomedcentral.com)
  • This is a sub-part (intracellular signaling peptides and proteins only) of List of MeSH codes (D12.776), itself a part of the list of the "D" codes for MeSH. (wikipedia.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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • The viral Bcl-2 protein promotes survival of infected cells and may contribute to the development of Kaposi sarcoma tumors [Boshoff, C. & Chang, Y. (2001) Annu. (nih.gov)
  • Hence, ABT-737 should prove efficacious in tumors with low Mcl-1 levels, or when combined with agents that inactivate Mcl-1, even to treat those tumors that overexpress Bcl-2. (nih.gov)
  • Comparison of KSHV Bcl-2 ( A ) to Bcl-x L ( B ) and to Bcl-2 ( C ). Residues of the hydrophobic groove that are homologous to those that contact the Bak and Bad peptides when complexed to Bcl-x L are shown along with the tryptophan residue of the NWGR sequence. (nih.gov)
  • 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)
  • 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)
  • RAS proteins are essential components of signalling pathways that emanate from cell surface receptors. (nih.gov)
  • A wealth of biochemical and genetic studies indicates that RAS proteins control a complex molecular circuitry that consists of a wide array of interconnecting pathways. (nih.gov)
  • Bax/Bak directly opens the VDAC to induce cytochrome c release, while Bcl-2/Bcl-xL closes this channel. (nih.gov)
  • Bcl-2/Bcl-xL inhibits Bid/Bik-induced cytochrome c release, probably through heterodimerization with Bid/Bik or by closing an unidentified channel(s). (nih.gov)
  • 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)
  • Both pharmacological factors, including inadequate drug concentration at the tumor site, and cellular factors can contribute to clinical resistance [ 2 ]. (biomedcentral.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)
  • 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)
  • 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)
  • Furthermore, the interacted protein of HULC and involved signaling pathway were investigated. (bvsalud.org)
  • 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 BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized. (nih.gov)
  • 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)
  • 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)
  • Based on the relative affinities (IC 50 in nM) of ABT-737 for mammalian pro-survival proteins, determined in solution competition assays (), ABT-737 and Bad bind to the same subset of Bcl-2 pro-survival proteins. (nih.gov)
  • Efficacy evaluation of ATO combined with CT on xenograft was carried in nude mice and related proteins were analysis by Immunohistochemistry assays. (biomedcentral.com)
  • Having established that the m41 proteins enhance MCMV replication in vivo, additional mutants were constructed in order to assess the relative contribution of the m41 proteins, and m41.1, to viral pathogenesis. (nih.gov)
  • 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)
  • A ) Backbone (N,C α ,C′) superposition of 10 low-energy NMR-derived structures for viral KSHV Bcl-2. (nih.gov)
  • Helices are numbered with respect to those observed in the structure of Bcl-x L . ( B ) Ribbon () depiction of the average-minimized structure for viral KSHV Bcl-2. (nih.gov)
  • C ) Solvent-accessible surface showing hydrophobic groove for viral KSHV Bcl-2. (nih.gov)
  • Viral Deoxyribonucleic acid (DNA) was extracted using Proteinase-K DNA Extraction method, and the presence of CMV and EBV-1 was detected by polymerase chain reaction and 2% agarose gel. (bvsalud.org)
  • 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)
  • Survival rate, cell apoptosis, cycle, expressions of related proteins, and caspase-3 activity were assessed to explore the effects of HULC on sensitivity of PCa cells to irradiation. (bvsalud.org)