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

PHD finger protein 11

PHF11, BCAP, PHD finger protein 11
Top mentioned proteins: DPP10, ADAM33, IgE, PI3K, Akt
Papers on PHF11
Vibrational spectroscopic methods for the overall quality analysis of washing powders.
Huck et al., Innsbruck, Austria. In Talanta, Mar 2016
For this purpose, principal component analysis (PCA) cluster models and partial least-squares (PLS) regression models were developed and different data pre-processing algorithms such as standard-normal-variate (SNV), multiplicative scatter correction (MSC), first derivative BCAP (db1), second derivative smoothing (ds2), smoothing Savitzky Golay 9 points (sg9) as well as different normalization procedures such as normalization between 0 and 1 (n01), normalization unit length (nle) or normalization by closure (ncl) were applied to reduce the influence of systematic disturbances.
Negative regulation of TLR signaling in myeloid cells-implications for autoimmune diseases.
Buckner et al., Seattle, United States. In Immunol Rev, Jan 2016
Here, we highlight three pathways that participate in inhibition of TLR responses in macrophages and DC, and their implications in autoimmunity; A20, encoded by the TNFAIP3 gene, Lyp encoded by the PTPN22 gene, and the BCAP/PI3K pathway.
IRF4 Deficiency Leads to Altered BCR Signalling Revealed by Enhanced PI3K Pathway, Decreased SHIP Expression and Defected Cytoskeletal Responses.
Lassila et al., Turku, Finland. In Scand J Immunol, Nov 2015
For example, the expression of B cell adaptor for PI3K (BCAP) was upregulated, whereas the SHIP (SH2-containing Inositol 5?-Phosphatase) expression was downregulated.
Tubulin inhibitor identification by bioactive conformation alignment pharmacophore-guided virtual screening.
Pae et al., Seoul, South Korea. In Chem Biol Drug Des, Nov 2015
To identify a novel small molecule that binds the αβ tubulin interface to affect microtubule dynamics, we developed a bioactive conformation alignment pharmacophore (BCAP) model to screen tubulin inhibitors from a huge database.
A functional AT/G polymorphism in the 5'-untranslated region of SETDB2 in the IgE locus on human chromosome 13q14.
Zhang et al., London, United Kingdom. In Genes Immun, Oct 2015
The immunoglobulin E (IgE)-associated locus on human chromosome 13q14 influencing asthma-related traits contains the genes PHF11 and SETDB2.
A Structural View of Negative Regulation of the Toll-like Receptor-Mediated Inflammatory Pathway.
Nussinov et al., İstanbul, Turkey. In Biophys J, Oct 2015
Structural data suggest that 1) Toll/IL-1R (TIR) domain-containing regulators (BCAP, SIGIRR, and ST2) interfere with TIR domain signalosome formation; 2) major deubiquitinases such as A20, CYLD, and DUBA prevent association of TRAF6 and TRAF3 with their partners, in addition to removing K63-linked ubiquitin chains that serve as a docking platform for downstream effectors; 3) alternative downstream pathways of TLRs also restrict signaling by competing to bind common partners through shared binding sites.
PHF11 expression and cellular distribution is regulated by the Toll-Like Receptor 3 Ligand Polyinosinic:Polycytidylic Acid in HaCaT keratinocytes.
Jones et al., Sydney, Australia. In Bmc Immunol, 2014
Polymorphisms in PHF11 have been associated with dermatitis and allergy and PHF11 regulates the transcription of T-cell cytokines as well as class switching to IgE in activated B-cells.
Nck-mediated recruitment of BCAP to the BCR regulates the PI(3)K-Akt pathway in B cells.
Batista et al., London, United Kingdom. In Nat Immunol, 2013
Here we found that Nck also controlled the phosphatidylinositol-3-OH kinase (PI(3)K)-kinase Akt pathway by recruiting the adaptor BCAP after activation of B cells.
Toll-like receptors, signaling adapters and regulation of the pro-inflammatory response by PI3K.
Pasare et al., Dallas, United States. In Cell Cycle, 2012
The recent discovery of BCAP as a TLR signaling adaptor, crucial for linking TLRs to PI3K activation, allows new questions of the importance of PI3K activation downstream of TLRs.
B-cell adaptor for PI3K (BCAP) negatively regulates Toll-like receptor signaling through activation of PI3K.
Hamerman et al., Seattle, United States. In Proc Natl Acad Sci U S A, 2012
BCAP is an essential activator of the PI3K pathway downstream of TLR signaling.
Role for B-cell adapter for PI3K (BCAP) as a signaling adapter linking Toll-like receptors (TLRs) to serine/threonine kinases PI3K/Akt.
Pasare et al., Dallas, United States. In Proc Natl Acad Sci U S A, 2012
BCAP is a unique TIR domain-containing toll like receptor (TLR) signaling adapter crucial for linking TLRs to PI3K activation and regulating the inflammatory response.
A requirement for the p85 PI3K adapter protein BCAP in the protection of macrophages from apoptosis induced by endoplasmic reticulum stress.
Greenberg et al., New York City, United States. In J Immunol, 2011
As macrophages engage their pathogenic targets, innate immune receptors trigger increased expression of BCAP, which endows them with the capacity to withstand further challenges from ongoing cellular insults, such as endoplasmic reticulum stress.
Allele-specific transcription of the asthma-associated PHD finger protein 11 gene (PHF11) modulated by octamer-binding transcription factor 1 (Oct-1).
Moffatt et al., Oxford, United Kingdom. In J Allergy Clin Immunol, 2011
the single nucleotide polymorphism rs1046295 of PHF11 modulates allele-specific binding by the octamer-binding transcription factor 1
Emergence of the PI3-kinase pathway as a central modulator of normal and aberrant B cell differentiation.
Rickert et al., Los Angeles, United States. In Curr Opin Immunol, 2011
The role of PI3K adaptor proteins (CD19, BCAP, and TC21) has also undergone revision to reflect both shared and unique properties.
Identification of BCAP-(L) as a negative regulator of the TLR signaling-induced production of IL-6 and IL-10 in macrophages by tyrosine phosphoproteomics.
Inoue et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2010
BCAP-(L) (but not BCAP-(S)) is a negative regulator of the TLR-mediated host defense system in macrophages.
Pathogenesis of allergic airway inflammation.
Shao et al., Omaha, United States. In Curr Allergy Asthma Rep, 2010
Several genes, including ADAM33, DPP10, PHF11, GPRA, TIM-1, PDE4D, OPN3, and ORMDL3, have been implicated in the pathogenesis and susceptibility to atopy and asthma.
ENU mutagenesis as a tool for understanding lung development and disease.
Dean et al., United Kingdom. In Biochem Soc Trans, 2009
Using the Harwell ENU sperm archive, we have recovered mouse lines harbouring mutations in the asthma-susceptibility genes Phf11 (PHD finger protein 11) and Dpp10 (dipeptidylpeptidase 10).
Contribution of BCAP to maintenance of mature B cells through c-Rel.
Kurosaki et al., Moriguchi, Japan. In Nat Immunol, 2003
Mice deficient in the B cell adaptor for phosphoinositide 3-kinase (BCAP) have reduced numbers of mature B lymphocytes, which show defects in cell survival and proliferation.
Positional cloning of a quantitative trait locus on chromosome 13q14 that influences immunoglobulin E levels and asthma.
Cookson et al., Oxford, United Kingdom. In Nat Genet, 2003
Positional cloning of a quantitative trait locus on chromosome 13q14 that influences immunoglobulin E levels and asthma.
BCAP: the tyrosine kinase substrate that connects B cell receptor to phosphoinositide 3-kinase activation.
Kurosaki et al., Moriguchi, Japan. In Immunity, 2000
Here, we report the identification of a novel B cell adaptor for phosphoinositide 3-kinase (PI3K), termed BCAP.
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