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

TRAF-interacting protein

This gene encodes a protein that contains an N-terminal RING finger motif and a putative coiled-coil domain. A similar murine protein interacts with TNFR-associated factor 1 (TRAF1), TNFR-associated factor 2 (TRAF2), and cylindromatosis. The interaction with TRAF2 inhibits TRAF2-mediated nuclear factor kappa-B, subunit 1 activation that is required for cell activation and protection against apoptosis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, SEI-1, ACID, HAD, TRIP-Br2
Papers on TRIP
TRIP-Br1 oncoprotein inhibits autophagy, apoptosis, and necroptosis under nutrient/serum-deprived condition.
Lee et al., Seoul, South Korea. In Oncotarget, Nov 2015
TRIP-Br1 oncogenic protein has been shown to have multiple biological functions in cells.
A Lentiviral Vector Expressing Japanese Encephalitis Virus-like Particles Elicits Broad Neutralizing Antibody Response in Pigs.
Desprès et al., Paris, France. In Plos Negl Trop Dis, Oct 2015
The efficiency of two lentiviral TRIP/JEV vectors expressing the JEV envelope prM and E glycoproteins at eliciting protective humoral response was assessed in a mouse model and piglets.
TRIP through the chromatin: a high throughput exploration of enhancer regulatory landscapes.
Akhtar et al., Novosibirsk, Russia. In Genomics, Sep 2015
Here, we discuss the potential of a powerful approach, TRIP, to study the functioning of enhancers in their native chromatin environments by introducing sensor constructs directly in the genome.
Tumor necrosis factor (TNF) receptor-associated factor (TRAF)-interacting protein (TRIP) negatively regulates the TRAF2 ubiquitin-dependent pathway by suppressing the TRAF2-sphingosine 1-phosphate (S1P) interaction.
Rho et al., Taejŏn, South Korea. In J Biol Chem, May 2015
TRAF-interacting protein (TRIP) is a known cellular binding partner of TRAF2 and inhibits TNF-induced NF-κB activation.
Renal safety of coformulated tenofovir/emtricitabine vs other nucleoside analogues in combination therapy in antiretroviral-naive patients aged 50 years or older in Spain: The TRIP study.
Blanco Ramos et al., In Hiv Clin Trials, 2015
OBJECTIVES: Our aim is to describe the impact of emtricitabine (FTC)/tenofovir (TDF) versus other nucleoside reverse transcriptase inhibitor (NRTIs)-based regimens on renal function of human immunodeficiency virus (HIV) naïve patients >50 years old who started combination antiretroviral therapy (cART).
Asymmetric fluorocyclizations of alkenes.
Gouverneur et al., Oxford, United Kingdom. In Acc Chem Res, 2015
Exchange of the tetrafluoroborate ions of Selectfluor with bulky lipophilic chiral anions (e.g., TRIP and derivatives) brings into solution the resulting chiral Selectfluor reagent, now capable of asymmetric fluorocyclization.
Methods for biomimetic remineralization of human dentine: a systematic review.
Chu et al., Hong Kong, Hong Kong. In Int J Mol Sci, 2014
A systematic search of the publications in the PubMed, TRIP, and Web of Science databases was performed.
Urinary biomarkers for the non-invasive diagnosis of endometriosis.
Hull et al., Auckland, New Zealand. In Cochrane Database Syst Rev, 2014
We searched the following databases to 20 April - 31 July 2015: CENTRAL, MEDLINE, EMBASE, CINAHL, PsycINFO, Web of Science, LILACS, OAIster, TRIP and
Transcriptional down-regulation of epidermal growth factor (EGF) receptors by nerve growth factor (NGF) in PC12 cells.
Lazarovici et al., Jerusalem, Israel. In J Mol Neurosci, 2014
Treatment with NGF also increased the cellular content of GCF2, a putative inhibitory transcription factor of the EGFR gene.
Identification of mutant genes with high-frequency, high-risk, and high-expression in lung adenocarcinoma.
Mei et al., Shanghai, China. In Thorac Cancer, 2014
Thyroid hormone receptor interactor (TRIP)12 was identified with the highest frequency.
Ablation of TRIP-Br2, a regulator of fat lipolysis, thermogenesis and oxidative metabolism, prevents diet-induced obesity and insulin resistance.
Kulkarni et al., Boston, United States. In Nat Med, 2013
Here we describe a new transcription co-regulator for adiposity and energy metabolism, SERTA domain containing 2 (TRIP-Br2, also called SERTAD2).
Aptamer-derived peptide inhibitors of Rho guanine nucleotide exchange factors.
Debant et al., Montpellier, France. In Enzymes, 2012
This is illustrated here by the first description of a peptide inhibitor of the oncogenic RhoGEF Tgat, TRIP(E32G), which is functional in vivo.
The TRAF-interacting protein (TRIP) is a regulator of keratinocyte proliferation.
Huber et al., Lausanne, Switzerland. In J Invest Dermatol, 2011
The TRAF-interacting protein (TRIP) is a regulator of keratinocyte proliferation.
Characterization of LRRFIP1.
Sullivan et al., Philadelphia, United States. In Biochem Cell Biol, 2010
LRRFIP1 is phosphorylated in response to immunologic stimuli and it is directed to lysosomal structures.
Transcription profiling in human platelets reveals LRRFIP1 as a novel protein regulating platelet function.
Bloodomics Consortium et al., Leicester, United Kingdom. In Blood, 2010
An association study of 6 of the 63 genes in 4235 cases and 6379 controls showed a putative association with myocardial infarction for COMMD7 (COMM domain-containing protein 7) and a major deviation from the null hypo thesis for LRRFIP1.
Modulation of TLR signaling by multiple MyD88-interacting partners including leucine-rich repeat Fli-I-interacting proteins.
Chen et al., In J Immunol, 2009
Immediately following lipopolysaccharide stimulation, both LRRFIP2 and Flap-1/LRRFIP1 compete with Fliih for interacting with MyD88 to activate the signaling.
The protein-tyrosine kinase Syk interacts with TRAF-interacting protein TRIP in breast epithelial cells.
Geahlen et al., West Lafayette, United States. In Oncogene, 2009
The overexpression of TRIP sensitizes cells to TNF-induced apoptosis, an effect that can be reversed by the coexpression of Syk.
The HIV-1 DNA flap stimulates HIV vector-mediated cell transduction in the brain.
Charneau et al., Paris, France. In Nat Biotechnol, 2001
Here we report that the insertion of this DNA flap sequence into HR vectors (TRIP vectors) improves gene transduction in neural cells, ex vivo and in vivo, in rat brain.
A signature motif in transcriptional co-activators mediates binding to nuclear receptors.
Parker et al., London, United Kingdom. In Nature, 1997
Ligand binding induces conformational changes in nuclear receptors and promotes their association with a diverse group of nuclear proteins, including SRC-1/p160, TIF-2/GRIP-1 and CBP/p300 which function as co-activators of transcription, and RIP-140, TIF-1 and TRIP-1/SUG-1 whose functions are unclear.
A WD-domain protein that is associated with and phosphorylated by the type II TGF-beta receptor.
Derynck et al., San Francisco, United States. In Nature, 1995
We have now identified a WD-domain-containing protein, TRIP-1, which specifically associates with the type II TGF-beta receptor in a kinase-dependent way.
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