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BCL2-associated athanogene 4

The protein encoded by this gene is a member of the BAG1-related protein family. BAG1 is an anti-apoptotic protein that functions through interactions with a variety of cell apoptosis and growth related proteins including BCL-2, Raf-protein kinase, steroid hormone receptors, growth factor receptors and members of the heat shock protein 70 kDa family. This protein contains a BAG domain near the C-terminus, which could bind and inhibit the chaperone activity of Hsc70/Hsp70. This protein was found to be associated with the death domain of tumor necrosis factor receptor type 1 (TNF-R1) and death receptor-3 (DR3), and thereby negatively regulates downstream cell death signaling. The regulatory role of this protein in cell death was demonstrated in epithelial cells which undergo apoptosis while integrin mediated matrix contacts are lost. Alternatively spliced transcript variants encoding distinct isoforms have been identified. [provided by RefSeq, Mar 2011] (from NCBI)
Top mentioned proteins: HSP70, bcl-2, CAN, HAD, HSP60
Papers on SODD
Annexin A7 modulates BAG4 and BAG4-binding proteins in mitochondrial apoptosis.
Tang et al., Dalian, China. In Biomed Pharmacother, Aug 2015
Furthermore, Annexin A7 was identified to form a complex with BAG4 which is a negative regulator of apoptosis.
The neuronal-specific SGK1.1 (SGK1_v2) kinase as a transcriptional modulator of BAG4, Brox, and PPP1CB genes expression.
Martín-Vasallo et al., Santa Cruz de Tenerife, Spain. In Int J Mol Sci, 2014
Further analysis of transcript and protein levels validated two genes: BCL2-associated athanogene 4 (BAG-4) and Brox.
FGFR1/3 tyrosine kinase fusions define a unique molecular subtype of non-small cell lung cancer.
Chen et al., Shanghai, China. In Clin Cancer Res, 2014
RESULTS: Of 1,328 tumors screened, two (0.2%) were BAG4-FGFR1 fusion and 15 (1.1%) were FGFR3-TACC3 fusion.
Expression profile of apoptosis-related genes potentially explains early recurrence after definitive chemoradiation in esophageal squamous cell carcinoma.
Lu et al., Chengdu, China. In Tumour Biol, 2014
Quantitative real-time polymerase chain reaction showed upregulation of BCLAF1 and downregulation of BAG4, CARD6, IGF1R, and TNF in the tissues of case patients, as compared with controls.
High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy.
Youle et al., Bethesda, United States. In Nature, 2014
We also discovered that HSPA1L (HSP70 family member) and BAG4 have mutually opposing roles in the regulation of parkin translocation.
Silencer of death domains controls cell death through tumour necrosis factor-receptor 1 and caspase-10 in acute lymphoblastic leukemia.
Bendall et al., Sydney, Australia. In Plos One, 2013
Consistent with this, expression of silencer of death domain (SODD) was reduced following NO-aspirin exposure and lentiviral mediated shRNA knockdown of SODD suppressed expansion of transduced cells confirming the importance of SODD for ALL cell survival.
Significance of SODD expression in childhood acute lymphoblastic leukemia and its influence on chemotherapy.
Zhu et al., Shantou, China. In Genet Mol Res, 2013
This study explored the clinical significance of silencer of death domain (SODD) expression in childhood acute lymphoblastic leukemia (ALL) and its influence on chemotherapy as well as the effect of SODD expression on apoptosis of leukemic cells.
Expression of Bcl-2 and the antiapoptotic BAG family proteins in ovarian cancer.
Grimm et al., Vienna, Austria. In Appl Immunohistochem Mol Morphol, 2013
The major aim of this study was to further define the expression pattern and the prognostic role of Bcl-2 together with BAG-1, BAG-3, and BAG-4 proteins in EOC patients receiving platinum/taxane-based chemotherapy.
MicroRNA-26a is strongly downregulated in melanoma and induces cell death through repression of silencer of death domains (SODD).
Shellman et al., Aurora, United States. In J Invest Dermatol, 2013
In surveying targets of miR-26a, we found that protein levels of SMAD1 (mothers against decapentaplegic homolog 1) and BAG-4/SODD were strongly decreased in sensitive cells treated with miR-26a mimic as compared with the control.
Loss of giant obscurins promotes breast epithelial cell survival through apoptotic resistance.
Kontrogianni-Konstantopoulos et al., Baltimore, United States. In Faseb J, 2012
Quantitative RT-PCR further indicated that the antiapoptotic genes BAG4 and HAX1 were up-regulated (1.5- and 1.4-fold, respectively), whereas initiator caspase-9 and death caspase-3 transcripts were down-regulated (0.8- and 0.6-fold, respectively).
Silencer of death domains (SODD) inhibits skeletal muscle and kidney enriched inositol 5-phosphatase (SKIP) and regulates phosphoinositide 3-kinase (PI3K)/Akt signaling to the actin cytoskeleton.
Mitchell et al., Australia. In J Biol Chem, 2011
Silencer of death domains (SODD) inhibits skeletal muscle and kidney enriched inositol 5-phosphatase (SKIP) and regulates phosphoinositide 3-kinase (PI3K)/Akt signaling to the actin cytoskeleton.
Transforming properties of 8p11-12 amplified genes in human breast cancer.
Ethier et al., Detroit, United States. In Cancer Res, 2010
We identified 21 candidate genes and provided evidence that three genes, namely, LSM-1, TC-1, and BAG4, have transforming properties when overexpressed.
[BAG family gene and its relationship with lung adenocarcinoma susceptibility].
Chen et al., Tianjin, China. In Zhongguo Fei Ai Za Zhi, 2010
RESULTS: The expression levels of BAG-1, BAG-2, BAG-5 in cancer tissues were significantly downregulated compared with matched pericancerous lung tissues and were protective factors of lung adenocarcinoma (P < 0.05, OR < 1); while the expression level of BAG-4 in cancer tissues were remarkably upregulated compared with the matched pericancerous lung tissues and was risk factor of lung adenocarcinoma (P < 0.05, OR > 1).
[Effects of SODD and survivin on leukemia cell apoptosis induced by chemotherapeutic drugs].
Hu et al., Wuhan, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2007
Vincristine induces Jurkat cell apoptosis by downregulating expression of SODD protein and priming the death receptor pathway.
A genome-wide linkage scan for cleft lip and cleft palate identifies a novel locus on 8p11-23.
Murray et al., Iowa City, United States. In Am J Med Genet A, 2007
results of analysis of the genome-wide scan data was a 20 cM region at 8p11-23 in which markers had LODs > or =1.0. Linkage and association analyses of these SNPs yield suggestive results for markers in FGFR1 and BAG4.
Multiple interacting oncogenes on the 8p11-p12 amplicon in human breast cancer.
Ethier et al., Ann Arbor, United States. In Cancer Res, 2007
Gene induces transformed phenotype when overexpressed in a cancer breast cell line.
Constitutive androstane receptor (CAR) ligand, TCPOBOP, attenuates Fas-induced murine liver injury by altering Bcl-2 proteins.
Gores et al., Rochester, United States. In Hepatology, 2006
The proapoptotic proteins Bak (Bcl-2 antagonistic killer) and Bax (Bcl-2-associated X protein) were depleted in livers from TCPOBOP-treated CAR+/+ mice.
Apoptosis: Silencing the death receptors.
Hofmann et al., Lausanne, Switzerland. In Curr Biol, 1999
An inhibitory protein has recently been identified, called silencer of death domains (SODD), that binds to the death domain of tumor necrosis factor receptor 1, thereby negatively regulating downstream signaling.
Prevention of constitutive TNF receptor 1 signaling by silencer of death domains.
Goeddel et al., San Francisco, United States. In Science, 1999
This apparent paradox may be explained by silencer of death domains (SODD), a widely expressed approximately 60-kilodalton protein that was found to be associated with the death domain of TNF-R1.
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