 Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
"Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Phosphoinositide phosphatases that catalyze the dephosphorylation (hydrolysis) of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) to produce PtdIns(3,4)P(2), which negatively regulates the PI3K ( 3-PHOSPHOINOSITIDE-DEPENDENT PROTEIN KINASES) pathways. They contain an SH2 DOMAIN and STERILE ALPHA MOTIF and have important functions in regulating the immune response and other cellular processes in vertebrates.
| Descriptor ID |
D000072183
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| MeSH Number(s) |
D08.811.277.352.650.624.750
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| Concept/Terms |
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Below are MeSH descriptors whose meaning is more general than "Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases".
Below are MeSH descriptors whose meaning is more specific than "Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases".
This graph shows the total number of publications written about "Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases" by people in this website by year, and whether "Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
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| 2001 | 0 | 1 | 1 | | 2005 | 0 | 1 | 1 | | 2010 | 0 | 1 | 1 | | 2011 | 0 | 1 | 1 | | 2015 | 0 | 1 | 1 | | 2016 | 1 | 0 | 1 | | 2017 | 0 | 1 | 1 | | 2019 | 1 | 0 | 1 |
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Below are the most recent publications written about "Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases" by people in Profiles.
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Franks SE, Getahun A, Cambier JC. A Precision B Cell-Targeted Therapeutic Approach to Autoimmunity Caused by Phosphatidylinositol 3-Kinase Pathway Dysregulation. J Immunol. 2019 06 15; 202(12):3381-3393.
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Getahun A, Wemlinger SM, Rudra P, Santiago ML, van Dyk LF, Cambier JC. Impaired B cell function during viral infections due to PTEN-mediated inhibition of the PI3K pathway. J Exp Med. 2017 04 03; 214(4):931-941.
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Getahun A, Beavers NA, Larson SR, Shlomchik MJ, Cambier JC. Continuous inhibitory signaling by both SHP-1 and SHIP-1 pathways is required to maintain unresponsiveness of anergic B cells. J Exp Med. 2016 05 02; 213(5):751-69.
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Akerlund J, Getahun A, Cambier JC. B cell expression of the SH2-containing inositol 5-phosphatase (SHIP-1) is required to establish anergy to high affinity, proteinacious autoantigens. J Autoimmun. 2015 Aug; 62:45-54.
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Waterman PM, Marschner S, Brandl E, Cambier JC. The inositol 5-phosphatase SHIP-1 and adaptors Dok-1 and 2 play central roles in CD4-mediated inhibitory signaling. Immunol Lett. 2012 Mar 30; 143(1):122-30.
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O'Neill SK, Getahun A, Gauld SB, Merrell KT, Tamir I, Smith MJ, Dal Porto JM, Li QZ, Cambier JC. Monophosphorylation of CD79a and CD79b ITAM motifs initiates a SHIP-1 phosphatase-mediated inhibitory signaling cascade required for B cell anergy. Immunity. 2011 Nov 23; 35(5):746-56.
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Zhang H, He J, Kutateladze TG, Sakai T, Sasaki T, Markadieu N, Erneux C, Prestwich GD. 5-Stabilized phosphatidylinositol 3,4,5-trisphosphate analogues bind Grp1 PH, inhibit phosphoinositide phosphatases, and block neutrophil migration. Chembiochem. 2010 Feb 15; 11(3):388-95.
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Crowley JE, Stadanlick JE, Cambier JC, Cancro MP. FcgammaRIIB signals inhibit BLyS signaling and BCR-mediated BLyS receptor up-regulation. Blood. 2009 Feb 12; 113(7):1464-73.
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Rider DA, Havenith CE, de Ridder R, Schuurman J, Favre C, Cooper JC, Walker S, Baadsgaard O, Marschner S, vandeWinkel JG, Cambier J, Parren PW, Alexander DR. A human CD4 monoclonal antibody for the treatment of T-cell lymphoma combines inhibition of T-cell signaling by a dual mechanism with potent Fc-dependent effector activity. Cancer Res. 2007 Oct 15; 67(20):9945-53.
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Brauweiler A, Merrell K, Gauld SB, Cambier JC. Cutting Edge: Acute and chronic exposure of immature B cells to antigen leads to impaired homing and SHIP1-dependent reduction in stromal cell-derived factor-1 responsiveness. J Immunol. 2007 Mar 15; 178(6):3353-7.
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