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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Protein tyrosine phosphatase, receptor type, J

BET
Top mentioned proteins: CAN, ACID, Histone, V1a, c-Myc
Papers on BET
Functional Genomic Landscape of Human Breast Cancer Drivers, Vulnerabilities, and Resistance.
New
Impact
Neel et al., Toronto, Canada. In Cell, Feb 2016
Finally, we demonstrate the utility of this large dataset by identifying BRD4 as a potential target in luminal breast cancer and PIK3CA mutations as a resistance determinant for BET-inhibitors.
Sustainable development of tyre char-based activated carbons with different textural properties for value-added applications.
New
McKay et al., Hong Kong, Hong Kong. In J Environ Manage, Feb 2016
The BET surface area, total pore volume and mesopore volume of the activated carbons from tyre char have been improved to 732 m(2)/g, 0.91 cm(3)/g and 0.89 cm(3)/g, respectively.
Preclinical anticancer efficacy of BET bromodomain inhibitors is determined by the apoptotic response.
New
Sims et al., United States. In Cancer Res, Feb 2016
UNASSIGNED: Small molecule inhibitors of the bromodomain and extraterminal (BET) family of proteins are being tested in clinical trials for a variety of cancers, but patient selection strategies remain limited.
Genome-Wide Profiling Reveals Remarkable Parallels Between Insertion Site Selection Properties of the MLV Retrovirus and the piggyBac Transposon in Primary Human CD4+ T Cells.
New
Ivics et al., Halle, Germany. In Mol Ther, Feb 2016
We demonstrate physical interaction between the PB transposase and BET-domain proteins (including BRD4), suggesting convergent evolution of a tethering mechanism that directs integrating genetic elements into TSSs.
CCAT1 is an enhancer-templated RNA that predicts BET sensitivity in colorectal cancer.
New
Firestein et al., In J Clin Invest, Feb 2016
To uncover the key epigenetic regulators that drive colon cancer growth, we used a CRISPR loss-of-function screen and identified a number of essential genes, including the bromodomain and extraterminal (BET) protein BRD4.
Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer.
New
Impact
Polyak et al., Boston, United States. In Nature, Feb 2016
BET bromodomain inhibitors, which have shown efficacy in several models of cancer, have not been evaluated in TNBC.
Molecular mechanisms of HIV latency.
Review
New
Peterlin et al., In J Clin Invest, Feb 2016
These proposed therapies include PKC and MAPK agonists as well as histone deacetylase inhibitors (HDACis) and bromodomain and extraterminal (BET) bromodomain inhibitors (BETis), which act synergistically to reactivate HIV in latently infected cells.
Integrated genomic characterization of IDH1-mutant glioma malignant progression.
New
Impact
Günel et al., New Haven, United States. In Nat Genet, Jan 2016
Our results not only provide mechanistic insight into the genetic and epigenetic mechanisms driving glioma progression but also identify inhibition of the bromodomain and extraterminal (BET) family as a potential therapeutic approach.
Composite microparticles of halloysite clay nanotubes bound by calcium carbonate.
New
Lvov et al., Ningbo, China. In J Colloid Interface Sci, Jan 2016
These microparticles have empty spherical structure and abundant pore distributions with maxima at 2.5, 3.9, 6.0 and 13.3nm, and higher surface area of 82.3m(2)g(-1) as characterized by SEM and BET test.
Bromodomains: Structure, function and pharmacology of inhibition.
Review
New
McKenna et al., Los Angeles, United States. In Biochem Pharmacol, Jan 2016
The demonstration in 2010 that two small molecule compounds, JQ1 and I-BET762, potently inhibit proteins of the bromodomain and extra-terminal (BET) family with translational potential for cancer and inflammatory disease sparked intense efforts in academia and pharmaceutical industry to develop novel bromodomain antagonists for therapeutic applications.
Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarcinoma.
New
Impact
Siveke et al., Stanford, United States. In Nat Med, Oct 2015
We show that JQ1, an inhibitor of the bromodomain and extraterminal (BET) family of proteins, suppresses PDAC development in mice by inhibiting both MYC activity and inflammatory signals.
Transcriptional plasticity promotes primary and acquired resistance to BET inhibition.
New
Impact
Zuber et al., Vienna, Austria. In Nature, Oct 2015
Following the discovery of BRD4 as a non-oncogene addiction target in acute myeloid leukaemia (AML), bromodomain and extra terminal protein (BET) inhibitors are being explored as a promising therapeutic avenue in numerous cancers.
BET bromodomain inhibitors in leukemia.
Review
New
Huntly et al., Cambridge, United Kingdom. In Exp Hematol, Aug 2015
The last few years have seen the identification of bromodomain and extraterminal (BET) proteins as critical mediators of transcription with effects on its direct control and cisregulation.
Beating the odds: BETs in disease.
Review
New
Filippakopoulos et al., Oxford, United Kingdom. In Trends Biochem Sci, Aug 2015
Recent developments targeting the bromo and extraterminal (BET) subset of BRD proteins demonstrated remarkable efficacy in murine models providing a compelling rationale for drug development and translation to the clinic.
Receptor-like tyrosine phosphatases CD45 and CD148 have distinct functions in chemoattractant-mediated neutrophil migration and response to S. aureus.
Impact
GeneRIF
Weiss et al., San Francisco, United States. In Immunity, 2011
CD45 and CD148 preferentially target different SFK members (Hck and Fgr versus Lyn, respectively) to positively and negatively regulate GPCR pathways.
Regulation of Src family kinases involved in T cell receptor signaling by protein-tyrosine phosphatase CD148.
GeneRIF
Brdicka et al., Praha, Czech Republic. In J Biol Chem, 2011
differential effects of CD148 in T cells and other leukocyte subsets
Protein-tyrosine phosphatase DEP-1 controls receptor tyrosine kinase FLT3 signaling.
GeneRIF
Müller et al., Jena, Germany. In J Biol Chem, 2011
DEP-1 is negatively regulating FLT3 signaling activity and that its loss may contribute to but is not sufficient for leukemogenic cell transformation.
CD148 enhances platelet responsiveness to collagen by maintaining a pool of active Src family kinases.
GeneRIF
Senis et al., Birmingham, United Kingdom. In J Thromb Haemost, 2010
CD148 plays a critical role in regulating GPVI/FcR gamma-chain expression and maintains a pool of active SFKs in platelets by directly dephosphorylating the C-terminal inhibitory tyrosines of SFKs that is essential for platelet activation
Polarized targeting of DNER into dendritic plasma membrane in hippocampal neurons depends on endocytosis.
GeneRIF
Kengaku et al., Wako, Japan. In J Neurochem, 2010
Our data suggest that clathrin-independent endocytosis is critical for the polarized targeting of somatodendritic proteins(DNER).
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