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

BCL2-like 2

Bcl-w, BCL2L2
This gene encodes a member of the BCL-2 protein family. The proteins of this family form hetero- or homodimers and act as anti- and pro-apoptotic regulators. Expression of this gene in cells has been shown to contribute to reduced cell apoptosis under cytotoxic conditions. Studies of the related gene in mice indicated a role in the survival of NGF- and BDNF-dependent neurons. Mutation and knockout studies of the mouse gene demonstrated an essential role in adult spermatogenesis. Alternative splicing results in multiple transcript variants. Read-through transcription also exists between this gene and the neighboring downstream PABPN1 (poly(A) binding protein, nuclear 1) gene. [provided by RefSeq, Dec 2010] (from NCBI)
Top mentioned proteins: bcl-2, Bcl-xL, Mcl-1, Bax, PrP
Papers on Bcl-w
Identification of a Novel Senolytic Agent, Navitoclax, Targeting the Bcl-2 Family of Anti-Apoptotic Factors.
Kirkland et al., Rochester, United States. In Aging Cell, Jan 2016
N targets Bcl-2, Bcl-xl, and Bcl-w, while T targets Bcl-2, Bcl-xl, and Mcl-1.
MiR-122 partly mediates the ochratoxin A-induced GC-2 cell apoptosis.
Luo et al., Beijing, China. In Toxicol In Vitro, Jan 2016
It showed that Bcl-w was down-regulated after OTA treatment, and caspase-3 was obviously activated.
Bcl-xL inhibition by molecular-targeting drugs sensitizes human pancreatic cancer cells to TRAIL.
Harada et al., Japan. In Oncotarget, Jan 2016
Both ABT-263 and ABT-737 inhibited the function of Bcl-2, Bcl-xL, and Bcl-w.
Bcl-2 family proteins as regulators of cancer cell invasion and metastasis: a review focusing on mitochondrial respiration and reactive oxygen species.
Um, Seoul, South Korea. In Oncotarget, Dec 2015
UNASSIGNED: Although Bcl-2 family proteins were originally identified as key regulators of apoptosis, an impressive body of evidence has shown that pro-survival members of the Bcl-2 family, including Bcl-2, Bcl-XL, and Bcl-w, can also promote cell migration, invasion, and cancer metastasis.
Sequence and expression variations in 23 genes involved in mitochondrial and non-mitochondrial apoptotic pathways and risk of oral leukoplakia and cancer.
Roy et al., Calcutta, India. In Mitochondrion, Nov 2015
Six SNPs (rs1473418 at BCL2; rs1950252 at BCL2L2; rs8190315 at BID; rs511044 at CASP1; rs2227310 at CASP7 and rs13010627 at CASP10) significantly modified risk of oral cancer but SNPs only at BCL2, CASP1and CASP10 modulated risk of leukoplakia.
Attacking cancer's Achilles heel: antagonism of anti-apoptotic BCL-2 family members.
Opferman, Memphis, United States. In Febs J, Sep 2015
To escape such death inducing signals, cancer cells often select for upregulation of anti-apoptotic BCL-2 family members including BCL-2, BCL-XL , BFL-1, BCL-W and MCL-1.
MicroRNA-203 Is a Prognostic Indicator in Bladder Cancer and Enhances Chemosensitivity to Cisplatin via Apoptosis by Targeting Bcl-w and Survivin.
Wang et al., Jinan, China. In Plos One, 2014
Western blotting and luciferase reporter assay showed Bcl-w and Survivin were direct downstream targets of miR-203.
Targeting BCL2-Proteins for the Treatment of Solid Tumours.
Vogler, Leicester, United Kingdom. In Adv Med, 2013
To this end, several strategies have been developed to inhibit BCL2, BCL-XL, BCL-w, and MCL1.
Cardio-miRNAs and onco-miRNAs: circulating miRNA-based diagnostics for non-cancerous and cancerous diseases.
Katoh, Tokyo, Japan. In Front Cell Dev Biol, 2013
BCL2L2, ß-catenin, BIM, CADM1, EZH2, FGFR1, NRAS, PTEN, TP53, and TWIST1 are representative miR-214 targets.
Anti-apoptotic BCL-2 family proteins in acute neural injury.
Prehn et al., Dublin, Ireland. In Front Cell Neurosci, 2013
We discuss overlapping and differential effects of the individual family members BCL-2, BCL-extra long (BCL-XL), myeloid cell leukemia 1 (MCL-1), and BCL2-like 2 (BCL-W) in the control of survival during development and pathophysiological processes such as trophic factor withdrawal, ischemic injury, excitotoxicity, oxidative stress and energy stress.
Bcl-w promotes cell invasion by blocking the invasion-suppressing action of Bax.
Um et al., Seoul, South Korea. In Cell Signal, 2012
By using human cancer cells and mouse embryonic fibroblasts, the study shows that BCL-W functions in the mitochondria to increase the levels of reactive oxygen species (ROS), which subsequently stimulates the invasion-promoting signaling pathway.
Targeting Bcl-2 family proteins in adult T-cell leukemia/lymphoma: in vitro and in vivo effects of the novel Bcl-2 family inhibitor ABT-737.
Tamura et al., Fukuoka, Japan. In Cancer Lett, 2012
Data show that ABT-737, a small molecule inhibitor of Bcl-2, Bcl-X(L), and Bcl-w, significantly induced apoptosis in HTLV-1 infected T-cell lines as well as in fresh adult T-cell leukemia/lymphoma (ATLL) cells.
Substantial susceptibility of chronic lymphocytic leukemia to BCL2 inhibition: results of a phase I study of navitoclax in patients with relapsed or refractory disease.
Humerickhouse et al., Melbourne, Australia. In J Clin Oncol, 2012
The novel BH3 mimetic navitoclax (ABT-263) specifically inhibits BCL2 and related proteins BCL-x(l) and BCL-w, potently inducing apoptosis of CLL cells in vitro.
miRNA-195 sensitizes human hepatocellular carcinoma cells to 5-FU by targeting BCL-w.
Lei et al., Hengyang, China. In Oncol Rep, 2012
miR-195 could improve the drug sensitivity at least in part by targeting Bcl-w to increase cell apoptosis in hepatocellular carcinoma cells.
Upregulated miR-29b promotes neuronal cell death by inhibiting Bcl2L2 after ischemic brain injury.
Jia et al., Shanghai, China. In Exp Brain Res, 2012
we verified that miR-29b directly targeted and inhibited Bcl2L2 gene expression
Crystal structure of a BCL-W domain-swapped dimer: implications for the function of BCL-2 family proteins.
Fairlie et al., Australia. In Structure, 2011
The alpha4-alpha5 hinge region is required for dimerization of BCL-W, and functioning of both pro- and antiapoptotic BCL-2 proteins.
Apoptosis and in vivo models to study the molecules related to this phenomenon.
Pantaleão et al., São Paulo, Brazil. In Einstein (sao Paulo), 2010
Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death.
The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.
Huang et al., Australia. In Cancer Cell, 2006
Despite its high affinity for Bcl-2, Bcl-x(L), and Bcl-w, many cell types proved refractory to ABT-737.
Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.
Letai et al., Boston, United States. In Cancer Cell, 2006
We show that the antiapoptotic proteins BCL-2, BCL-XL, MCL-1, BFL-1, and BCL-w each bear a unique pattern of interaction with a panel of peptides derived from BH3 domains of BH3-only proteins.
An inhibitor of Bcl-2 family proteins induces regression of solid tumours.
Rosenberg et al., San Diego, United States. In Nature, 2005
Here, using nuclear magnetic resonance (NMR)-based screening, parallel synthesis and structure-based design, we have discovered ABT-737, a small-molecule inhibitor of the anti-apoptotic proteins Bcl-2, Bcl-X(L) and Bcl-w, with an affinity two to three orders of magnitude more potent than previously reported compounds.
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