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

BID BH3 interacting domain death agonist

BH3 Interacting Domain Death Agonist, BID
Top mentioned proteins: HAD, PrP, CAN, bcl-2, Bax
Papers using BH3 Interacting Domain Death Agonist antibodies
Human and murine granzyme B exhibit divergent substrate preferences
Martin Seamus J. et al., In The Journal of Cell Biology, 1999
... The following antibodies were used: anti–caspase-3, anti–human caspase-7, anti-XIAP, and anti–human BID (BD Biosciences); anti–mouse caspase-7 (Millipore); anti–mouse ...
Caspase cleavage product of BAP31 induces mitochondrial fission through endoplasmic reticulum calcium signals, enhancing cytochrome c release to the cytosol
Shore Gordon C. et al., In The Journal of Cell Biology, 1995
... BAX aa 1–21 (Upstate Biotechnology); Rabbit pAb raised against the p15 caspase cleavage product of BID and purified by affinity selection; and mouse mAbs to pigeon cyt.c (BD Biosciences), chicken α-tubulin (clone DM1A; ...
Papers on BH3 Interacting Domain Death Agonist
Investigation of selective JAK1 inhibitor GSK2586184 for the treatment of psoriasis in a randomized placebo-controlled Phase 2a study.
Griffiths et al., Stevenage, United Kingdom. In Br J Dermatol, Feb 2016
METHODS: Sixty patients with moderate to severe plaque psoriasis were randomized to Cohort A; 100 mg, 200 mg or 400 mg GSK2586184 twice daily (BID) or placebo, and 8 were in open label Cohort B, a small exploratory cohort treated with 400 mg GSK2586184 BID to explore differential gene expresssion.
Human islet cells are killed by BID-independent mechanisms in response to FAS ligand.
Thomas et al., Sydney, Australia. In Apoptosis, Feb 2016
The BH3-only protein BID is activated in the BCL-2-regulated or mitochondrial apoptosis pathway and acts as a switch between the extrinsic and intrinsic cell death pathways.
Once-daily liraglutide (1.2 mg) compared with twice-daily exenatide (10 µg) in the treatment of type 2 diabetes patients: An indirect treatment comparison meta-analysis.
Adena et al., Sydney, Australia. In J Diabetes, Feb 2016
In a randomized head-to-head trial, liraglutide 1.8 mg once daily (OD) led to greater reductions in glycated hemoglobin (HbA1c ) level than exenatide 10 µg twice daily (BID).
Small bowel protection against NSAID-injury in rats: Effect of rifaximin, a poorly absorbed, GI targeted, antibiotic.
Scarpignato et al., Pisa, Italy. In Pharmacol Res, Jan 2016
The present study examined the enteroprotective effects of a delayed-release formulation of rifaximin-EIR (R-EIR, 50mg/kg BID, i.g.), a poorly absorbed antibiotic with a broad spectrum of antibacterial activity, in a rat model of enteropathy induced by indomethacin (IND, 1.5mg/kg BID for 14 days) administration.
Dual modulation of Ras-Mnk and PI3K-AKT-mTOR pathways: A Novel c-FLIP inhibitory mechanism of 3-AWA mediated translational attenuation through dephosphorylation of eIF4E.
Goswami et al., New Delhi, India. In Sci Rep, Dec 2015
Moreover, the suppression of c-FLIP due to inhibition of translation initiation complex by 3-AWA enhanced FAS trafficking, BID and caspase 8 cleavage.
A review of head-to-head comparisons of GLP-1 receptor agonists.
Madsbad, Hvidovre, Denmark. In Diabetes Obes Metab, Nov 2015
These fall into two classes based on their receptor activation: short-acting exenatide twice daily (BID) and lixisenatide once daily (OD); and longer-acting liraglutide OD, exenatide once weekly (OW), albiglutide OW and dulaglutide OW.
An interconnected hierarchical model of cell death regulation by the BCL-2 family.
Cheng et al., Kettering, United States. In Nat Cell Biol, Oct 2015
Using combinatorial gain-of-function and loss-of-function approaches in Bid(-/-)Bim(-/-)Puma(-/-)Noxa(-/-) and Bax(-/-)Bak(-/-) cells, we have constructed an interconnected hierarchical model that accommodates and explains how the intricate interplays between the BCL-2 members dictate cellular survival versus death.
Apoptosis in mammalian oocytes: a review.
Chaube et al., Benares, India. In Apoptosis, Aug 2015
BID, a BH3-only protein act as a bridge between both apoptotic pathways and its cleavage activates cell death machinery of both the pathways inside the follicular microenvironment.
Pharmacokinetics of crizotinib in NSCLC patients.
Burghuber et al., Vienna, Austria. In Expert Opin Drug Metab Toxicol, May 2015
EXPERT OPINION: Crizotinib is administered orally as a capsule and clinical studies indicated 250 mg crizotinib BID continuously as the maximal tolerated dose in cancer patients.
Emerging new therapies for the treatment of type 2 diabetes mellitus: glucagon-like peptide-1 receptor agonists.
Taylor et al., Gainesville, United States. In Clin Ther, Apr 2015
The newer once-weekly formulations are more convenient than the BID and once-daily medications, which could improve adherence and may be more attractive to providers and patients.
Systematic review of tofacitinib: a new drug for the management of rheumatoid arthritis.
Kaushal et al., Ludhiāna, India. In Clin Ther, 2014
The results of the Phase II trials show that tofacitinib at doses ≥3 mg BID was efficacious among the nonresponders.
Proteasome inhibitors evoke latent tumor suppression programs in pro-B MLL leukemias through MLL-AF4.
Hsieh et al., New York City, United States. In Cancer Cell, 2014
Specifically, in MLL pro-B lymphoid, but not myeloid, leukemias, proteasome inhibition triggers apoptosis and cell cycle arrest involving activation cleavage of BID by caspase-8 and upregulation of p27, respectively.
The ATM-BID pathway regulates quiescence and survival of haematopoietic stem cells.
Gross et al., Israel. In Nat Cell Biol, 2012
BID, a BH3-only BCL2 family member, functions in apoptosis as well as the DNA-damage response.
Non-apoptotic role of BID in inflammation and innate immunity.
Saleh et al., Montréal, Canada. In Nature, 2011
Our results reveal a significant crosstalk between innate immunity and apoptosis and identify BID, a BCL2 family protein, as a critical component of the inflammatory response.
BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program.
Cheng et al., Saint Louis, United States. In Science, 2011
We provide in vivo evidence demonstrating an essential role of the proteins BID, BIM, and PUMA in activating BAX and BAK.
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