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*  Similar papers for Erratum to: BAK, BAX, and NBK/BIK Proapoptotic Gene Alterations in Iranian Patients with Ataxia...
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 manufacturer's instructions (Applied Biosystems). Eight of fifty Iranian AT patients (16%)
  https://www.semanticscholar.org/paper/Erratum-to-BAK-BAX-and-NBK-BIK-Proapoptotic-Gene-A-Isaian-Bogdanova/5ff362a0b0d4621bb975a98f9ae9610ff70adbb1?tab=relatedPapers
*  The mitochondrial protein Bak is pivotal for gliotoxin-induced apoptosis and a critical host factor of Aspergillus fumigatus...
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 ...
  http://jcb.rupress.org/content/174/4/509
*  Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death | Science
Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax andBak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, ...
  http://science.sciencemag.org/content/292/5517/727
*  BAX/BAK-Independent Mitoptosis during Cell Death Induced by Proteasome Inhibition?
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.
  http://pubmedcentralcanada.ca/pmcc/articles/PMC2927846/
*  Mitochondria and cell death: outer membrane permeabilization and beyond.
Abstract Mitochondrial outer membrane permeabilization (MOMP) is often required for activation of the caspase proteases that cause apoptotic cell death. Various intermembrane space..
  https://www.omicsonline.org/references/mitochondria-and-cell-death-outer-membrane-permeabilization-and-beyond-600600.html
*  Inhibition of the ER Ca2+ pump forces multidrug-resistant cells deficient in Bak and Bax into necrosis | Journal of Cell Science
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, ...
  http://jcs.biologists.org/content/122/24/4481
*  Dry Eye Treatment
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. It's 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 ...
  http://www.greatfallseyecare.com/Content/EyeConditions/dryeye/dry_eye.aspx
*  Dry Eye Treatment
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. It's 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 ...
  http://www.visionplusvero.com/Content/EyeConditions/dryeye/dry_eye.aspx
*  Anti BAK Antibody, clone AB04/1A2 (PrecisionAb™ Monoclonal Antibody) | Bio-Rad Antibodies (formerly AbD Serotec)
Mouse anti Human BAK antibody recognizes the Bcl-2 homologous antagonist/killer, also known as BAK, BCL2-like 7 protein, apoptosis regulat
  https://www.bio-rad-antibodies.com/human-bak-antibody-ab04-1a2-vma00527.html
*  Bax and Bak are localized to the ER in addition to thei | Open-i
Bax and Bak are localized to the ER in addition to their mitochondrial location. (A) Wild-type and bax−/−bak−/− MEFs as well as HeLa cells were resuspen
  https://openi.nlm.nih.gov/detailedresult.php?img=PMC2172724_200302084f1b&req=4
*  Plus it
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 ...
  http://cancerdiscovery.aacrjournals.org/content/early/2016/07/22/2159-8290.CD-RW2016-136
*  THE POTENTIAL DICHOTOMOUS ROLE OF ACTIVATING TRANSCRIPTION FACTOR 3 (ATF3) IN COLON CANCER
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 ...
  https://drum.lib.umd.edu/handle/1903/17382
*  Most recent papers with the keyword Cancer and THR | Read by QxMD
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 ...
  https://www.readbyqxmd.com/keyword/60105
*  The VDAC2-BAK axis regulates peroxisomal membrane permeability | JCB
The BCL-2 family proteins, consisting of both antiapoptotic and proapoptotic members, are the major regulators of mammalian apoptosis (Czabotar et al., 2014). BAK and BAX are mutually redundant effectors of cell death, and either protein is sufficient to trigger apoptosis in response to apoptotic signals (Wei et al., 2001). The BCL-2 family proteins are known to localize to mitochondria and the ER (Scorrano et al., 2003; Zong et al., 2003). Most studies have focused on how the BCL-2 proteins function on mitochondria. Upon apoptotic stimuli, BAK and BAX are activated by activator BH3-only molecules to induce MOMP, thereby causing the release of apoptogenic ...
  http://jcb.rupress.org/content/early/2017/02/06/jcb.201605002
*  Inhibitor of Apoptosis
Ca2+-mediated mitochondrial permeability transition (mPT) is the final common pathway of stress-induced cell death in many major pathologies, but its regulation in intact cells is poorly understood. it has been suggested that Bcl-2 overexpression or reduction of Bax/Bak expression can mediate protective effect by diminishing mitochondrial Ca2+ ([Ca2+]m) load from the endoplasmic reticulum (ER) Ca2+… Continue reading Ca2+-mediated mitochondrial permeability transition (mPT) is the final common pathway of. ...
  http://www.research-in-field.com/category/inhibitor-of-apoptosis/
*  KEGG PATHWAY: Apoptosis - Homo sapiens (human)
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 ...
  http://www.genome.jp/kegg-bin/show_pathway?133827084014083/hsa04210.args
*  KEGG PATHWAY: Apoptosis - Homo sapiens (human)
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 ...
  http://www.genome.jp/kegg-bin/show_pathway?hsa04210+7124
*  KEGG PATHWAY: Apoptosis - Mus musculus (mouse)
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 ...
  http://www.genome.jp/kegg-bin/show_pathway?mmu04210+282322
*  Plus it
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 ...
  http://cancerres.aacrjournals.org/content/64/5/1703
*  BAK | Article about BAK by The Free Dictionary
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
  http://encyclopedia2.thefreedictionary.com/BAK
*  The conserved N‐terminal BH4 domain of Bcl‐2 homologues is essential for inhibition of apoptosis and interaction with CED‐4 |...
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).. ...
  http://emboj.embopress.org/content/17/4/1029
*  OriGene - BAK1 (NM 001188) shRNA
BAK1 - BAK1 - Human, 4 unique 29mer shRNA constructs in retroviral untagged vector shRNA available for purchase from OriGene - Your Gene Company.
  http://www.origene.com/shRNA/TR314515.aspx
*  Oticin HC (BAK Free) Otic (Ear) : Uses, Side Effects, Interactions, Pictures, Warnings & Dosing - WebMD
Find patient medical information for Oticin HC (BAK Free) Otic (Ear) on WebMD including its uses, side effects and safety, interactions, pictures, warnings and user ratings.
  http://www.webmd.com/drugs/2/drug-152665/oticin-hc-bak-free-otic-ear/details
*  KORENDY Türkiye - Kore Cilt Bakım ve Kozmetik Ürünleri - KBeauty - Korendy Turkiye
Güney Kore'den orjinal ve en seçkin cilt bakım ürünleri artık Türkiye'de. Bol bol bedava tester. 1~3 günde teslimat. Sevgi dolu müşteri hizmetleri ^_^
  https://www.korendy.com.tr/
*  Bak抗体[AT8B4]|Abcam中国|Anti-Bak抗体[AT8B4]
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。
  http://www.abcam.cn/bak-antibody-at38e2-ab104124.html