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

Myotubularin related protein 6

MTMR6, myotubularin-related protein 6
Top mentioned proteins: MTMR3, MTMR2, MTM1, V1a, STAT1
Papers on MTMR6
miR-190b is markedly upregulated in the intestine in response to simian immunodeficiency virus replication and partly regulates myotubularin-related protein-6 expression.
Lackner et al., Laos. In J Immunol, 2014
In contrast, mRNA expression of myotubularin-related protein 6 (MTMR6), a negative regulator of CD4(+) T cell activation/proliferation, significantly decreased in SIV-infected macrophages.
Sequential breakdown of 3-phosphorylated phosphoinositides is essential for the completion of macropinocytosis.
Arai et al., Tokyo, Japan. In Proc Natl Acad Sci U S A, 2014
By making use of information in the Caenorhabditis elegans mutants defective in fluid-phase endocytosis, we found that mammalian phosphoinositide phosphatase MTMR6 that dephosphorylates PI(3)P to PI, and its binding partner MTMR9, are required for macropinocytosis.
Use of proteomic analysis tools to identify HCV-proteins down-regulated by acetylsalicylic acid.
Rivas-Estilla et al., In Ann Hepatol, 2013
Among proteins differentially expressed in Huh7-HCV cells, we found proteins related to cell proliferation (MTMR6, FAM22, HDGF and HCF-1) after 24 h of ASA treatment; and upregulation of angiostatin, PI4KA and STAT-1 after 48 h of treatment.
Phosphatidylinositol 3-phosphatase myotubularin-related protein 6 (MTMR6) is regulated by small GTPase Rab1B in the early secretory and autophagic pathways.
Hamakubo et al., Tokyo, Japan. In J Biol Chem, 2013
We prepared anti-myotubularin-related protein 6 (MTMR6) monoclonal antibody and used it to study the regulatory mechanism of MTMR6.
Myotubularin-related protein (MTMR) 9 determines the enzymatic activity, substrate specificity, and role in autophagy of MTMR8.
Wilson et al., Saint Louis, United States. In Proc Natl Acad Sci U S A, 2012
We studied a subfamily of homologous myotubularins, including myotubularin-related protein 6 (MTMR6), MTMR7, and MTMR8, all of which dimerize with the catalytically inactive MTMR9.
MTMR9 increases MTMR6 enzyme activity, stability, and role in apoptosis.
Majerus et al., Saint Louis, United States. In J Biol Chem, 2009
MTMR9 greatly enhances the functions of MTMR6
KCa3.1 potassium channels are critical for cAMP-dependent chloride secretion and cyst growth in autosomal-dominant polycystic kidney disease.
Skolnik et al., New York City, United States. In Kidney Int, 2008
Net chloride secretion was enhanced by the KCa3.1 activator DCEBIO and both chloride secretion and in vitro cyst growth were inhibited by overexpression of myotubularin-related protein-6, a phosphatase that specifically inhibits KCa3.1 channel activity.
Specificity of the myotubularin family of phosphatidylinositol-3-phosphatase is determined by the PH/GRAM domain.
Skolnik et al., New York City, United States. In J Biol Chem, 2006
We recently found that MTMR6 specifically inhibits the Ca2+-activated K+ channel, KCa3.1, by dephosphorylating PI(3)P.
Phosphatidylinositol-3 phosphatase myotubularin-related protein 6 negatively regulates CD4 T cells.
Skolnik et al., New York City, United States. In Mol Cell Biol, 2006
Data show that KCa3.1, which is critical for Ca2+ influx in reactivated naive T cells and central memory T cells, requires phosphatidylinositol-3 phosphatase for activation and is inhibited by PI(3)P phosphatase myotubularin-related protein 6 (MTMR6).
Phosphatidylinositol 3-phosphate indirectly activates KCa3.1 via 14 amino acids in the carboxy terminus of KCa3.1.
Skolnik et al., New York City, United States. In Mol Biol Cell, 2006
We recently found that the KCa3.1 channel also specifically requires phosphatidylinositol-3 phosphate [PI(3)P] for channel activity and is inhibited by myotubularin-related protein 6 (MTMR6), a PI(3)P phosphatase.
The phosphatidylinositol 3-phosphate phosphatase myotubularin- related protein 6 (MTMR6) is a negative regulator of the Ca2+-activated K+ channel KCa3.1.
Skolnik et al., New York City, United States. In Mol Cell Biol, 2005
We identified a Ca(2+)-activated K channel, K(Ca)3.1 (also known as KCa4, IKCa1, hIK1, or SK4), that specifically interacts with the MTMR6 subfamily of MTMs via coiled coil (CC) domains on both proteins.
Identification of myotubularin as the lipid phosphatase catalytic subunit associated with the 3-phosphatase adapter protein, 3-PAP.
Mitchell et al., Melbourne, Australia. In Proc Natl Acad Sci U S A, 2003
Identification of myotubularin as the lipid phosphatase catalytic subunit associated with the 3-phosphatase adapter protein, 3-PAP.
The resistance of B-CLL cells to DNA damage-induced apoptosis defined by DNA microarrays.
Delic et al., Fontenay-aux-Roses, France. In Blood, 2003
In this manner, in 11 sensitive and 11 resistant B-CLL cell samples tested, 13 genes were found to be specific for all resistant samples: nuclear orphan receptor TR3, major histocompatibility complex (MHC) class II glycoprotein HLA-DQA1, mtmr6, c-myc, c-rel, c-IAP1, mat2A, and fmod were up-regulated, whereas MIP1a/GOS19-1 homolog, stat1, blk, hsp27, and ech1 were down-regulated.
Phosphatidylinositol-5-phosphate activation and conserved substrate specificity of the myotubularin phosphatidylinositol 3-phosphatases.
Barr et al., Martinsried, Germany. In Curr Biol, 2003
investigation of MTM1 and MTMR6 and finding that they use PtdIns(3,5)P2 in addition to PtdIns3P as a substrate in vitro
Myotubularin and MTMR2, phosphatidylinositol 3-phosphatases mutated in myotubular myopathy and type 4B Charcot-Marie-Tooth disease.
Dixon et al., Ann Arbor, United States. In J Biol Chem, 2002
Furthermore, the MTM-related phosphatases MTMR1, MTMR3, and MTMR6 also dephosphorylate PI(3)P, suggesting that activity toward this substrate is common to all myotubularin family enzymes.
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