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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

BCL2-associated agonist of cell death

The protein encoded by this gene is a member of the BCL-2 family. BCL-2 family members are known to be regulators of programmed cell death. This protein positively regulates cell apoptosis by forming heterodimers with BCL-xL and BCL-2, and reversing their death repressor activity. Proapoptotic activity of this protein is regulated through its phosphorylation. Protein kinases AKT and MAP kinase, as well as protein phosphatase calcineurin were found to be involved in the regulation of this protein. Alternative splicing of this gene results in two transcript variants which encode the same isoform. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: bcl-2, Akt, PrP, CAN, V1a
Papers using BAD antibodies
Cytolytic T lymphocyte-associated antigen-4 and the TcRζ/CD3 complex, but not CD28, interact with clathrin adaptor complexes AP-1 and AP-2.
Wölfl Stefan, In PLoS ONE, 1998
... Anti-phospho-GSK-3 α/β and anti-BAD mAbs were purchased from New England Biolabs (Hertfordshire, UK), anti-GSK-3 α/β ...
Papers on BAD
A single 60-min bout of peristaltic pulse external pneumatic compression transiently upregulates phosphorylated ribosomal protein s6.
Roberts et al., Auburn, United States. In Clin Physiol Funct Imaging, Feb 2016
Notable decreases also included p-BAD (Ser112; -28%, P = 0·004) at 4 h post-EPC compared to PRE levels.
Preclinical anticancer efficacy of BET bromodomain inhibitors is determined by the apoptotic response.
Sims et al., United States. In Cancer Res, Feb 2016
We further reveal that the expression signatures of the apoptotic genes BCL2, BCL2L1, and BAD significantly predict response to BETi.
Repurposing L-Menthol for Systems Medicine and Cancer Therapeutics? L-Menthol Induces Apoptosis through Caspase 10 and by Suppressing HSP90.
Shasany et al., Lucknow, India. In Omics, Jan 2016
The proteomics analyses showed downregulation of HSP90 protein (also corroborated by its low transcript abundance), which in turn indicated inhibition of AKT-mediated survival pathway, release of pro-apoptotic factor BAD from BAD and BCLxL complex, besides regulation of other factors related to apoptosis.
RanBP3 Regulates Melanoma Cell Proliferation via Selective Control of Nuclear Export.
Wagner et al., Vienna, Austria. In J Invest Dermatol, Jan 2016
Rendering mechanistic support to RanBP3 silencing-mediated apoptosis, consequent to extracellular signal-regulated kinase nuclear entrapment, we observed increased levels of cytoplasmically restricted nonphosphorylated/active proapoptotic Bcl-2-antagonist of cell death (BAD) protein.
The p70S6K Specific Inhibitor PF-4708671 Impedes Non-Small Cell Lung Cancer Growth.
Li et al., Chengdu, China. In Plos One, Dec 2015
Diametrically opposite, the downstream protein levels of BAD, Caspase3 and ERK had increased after treatment with PF-4708671.
Bile Acid diarrhea: prevalence, pathogenesis, and therapy.
Camilleri, Rochester, United States. In Gut Liver, Jun 2015
Bile acid diarrhea (BAD) is usually seen in patients with ileal Crohn's disease or ileal resection.
BH3-only proteins: a 20-year stock-take.
Puthalakath et al., Melbourne, Australia. In Febs J, Mar 2015
Since the discovery of the first BH3-only protein BAD almost 20 years ago, at least seven more BH3-only proteins have been identified in mammals.
Bile acid diarrhoea and FGF19: new views on diagnosis, pathogenesis and therapy.
Walters, London, United Kingdom. In Nat Rev Gastroenterol Hepatol, 2014
Increasing evidence, including that from several large case series using SeHCAT (selenium homocholic acid taurine) tests for diagnosis, indicates that bile acid diarrhoea (BAD) accounts for a sizeable proportion of patients who would otherwise be diagnosed with IBS.
Regulation of hepatic energy metabolism and gluconeogenesis by BAD.
Danial et al., Boston, United States. In Cell Metab, 2014
We show that the physiologic balance of hepatic glycolysis and gluconeogenesis is regulated by Bcl-2-associated agonist of cell death (BAD), a protein with roles in apoptosis and metabolism.
Nitric oxide as a mediator of estrogen effects in osteocytes.
Pilz et al., San Diego, United States. In Vitam Horm, 2013
Moreover, we found that 17β-estradiol protects osteocytes against apoptosis via the NO/cGMP signaling pathway: type II PKG mediates estradiol-induced activation of the prosurvival kinases Erk and Akt, whereas type I PKG contributes to prosurvival signaling by directly phosphorylating and inactivating the cell death protein BAD.
[Concept, pathophysiology and treatment for branch atheromatous disease].
Yamamoto, Kyoto, Japan. In Rinsho Shinkeigaku, 2013
Small deep brain infarcts are often caused by two different vascular pathologies: 1. atheromatous occlusion at the orifice of large caliber penetrating arteries termed branch atheromatous disease (BAD) and 2. lipohyallinotic degenerative changes within the course of penetrating arteries termed lipohyalinitic degeneration.
Inactivation of BAD by IKK inhibits TNFα-induced apoptosis independently of NF-κB activation.
Lin et al., Chicago, United States. In Cell, 2013
Here, we report that inactivation of the BH3-only protein BAD by IKK independently of NF-κB activation suppresses TNFα-induced apoptosis.
p38MAPK suppresses chronic pancreatitis by regulating HSP27 and BAD expression.
Sakurai et al., Ōsaka, Japan. In Free Radic Biol Med, 2012
p38MAPK suppresses chronic pancreatitis by upregulating HSP27 expression and downregulating BAD expression.
Differences in the mechanisms of proapoptotic BH3 proteins binding to Bcl-XL and Bcl-2 quantified in live MCF-7 cells.
Andrews et al., Hamilton, Canada. In Mol Cell, 2012
mechanism of proapoptotic BH3 proteins Bad and Bid binding to Bcl-XL and Bcl-2 in breast cancer cells
A moderate decline in U937 cell GSH levels triggers PI3 kinase/Akt-dependent Bad phosphorylation, thereby preventing an otherwise prompt apoptotic response.
Cantoni et al., Urbino, Italy. In Pharmacol Res, 2012
A mild redox imbalance associated with a slight reduction of the GSH pool commits U937 cells to apoptosis, however prevented by events leading to PI3K/Akt-dependent mitochondrial loss of BAD.
Upregulation of BAD, a pro-apoptotic protein of the BCL2 family, in vascular smooth muscle cells exposed to uremic conditions.
Galmiche et al., France. In Biochem Biophys Res Commun, 2012
the regulation of BAD by uremic toxins and report the sensitization of vascular smooth muscle cells to apoptosis upon BAD induction was explored.
URI is an oncogene amplified in ovarian cancer cells and is required for their survival.
Krek et al., Zürich, Switzerland. In Cancer Cell, 2011
Here we identify URI, which encodes a mitochondrial inhibitor of PP1γ and PP1γ-mediated feedback inhibition of S6K1-BAD survival signaling, as an oncogene amplified and overexpressed in ovarian cancer cell lines and human ovarian carcinomas.
BAD modulates counterregulatory responses to hypoglycemia and protective glucoprivic feeding.
Danial et al., Boston, United States. In Plos One, 2010
BAD modulates counterregulatory responses to hypoglycemia and protective glucoprivic feeding
When BAD is good for beta cells.
Roe et al., Chicago, United States. In Cell Metab, 2008
BAD, a proapoptotic member of the Bcl-2 family of proteins, is regulated by phosphorylation.
Dual role of proapoptotic BAD in insulin secretion and beta cell survival.
Korsmeyer et al., Boston, United States. In Nat Med, 2008
These findings provide genetic proof of the bifunctional activities of BAD in both beta cell survival and insulin secretion.
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