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

TGFB1-induced anti-apoptotic factor 1

MYO18A, TIAF1, SP-R210, MysPDZ, myosin XVIIIA
Top mentioned proteins: V1a, Actin, SP-A, HAD, CAN
Papers using MYO18A antibodies
STK35L1 associates with nuclear actin and regulates cell cycle and migration of endothelial cells
Chang N-S et al., In Cell Death & Disease, 2010
... tubulin (Sigma) and TIAF1 (Abcam).
Papers on MYO18A
Genome-wide pathway analysis of a genome-wide association study on Alzheimer's disease.
Song et al., Seoul, South Korea. In Neurol Sci, 2015
The strongest hypothetical biological mechanism was rs8076604 [non-synonymous coding (deleterious)] to MYO18A to negative regulation of programmed cell death [nominal P < 0.001, false discovery rate (FDR) <0.043].
SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation.
Chroneos et al., United States. In Plos One, 2014
The surfactant protein (SP-A) receptor SP-R210 has been shown to increase phagocytosis of SP-A-bound pathogens and to modulate cytokine secretion by immune cells.
The GOLPH3 pathway regulates Golgi shape and function and is activated by DNA damage.
Field et al., San Diego, United States. In Front Neurosci, 2014
The Golgi protein GOLPH3 binds to PtdIns(4)P and MYO18A, linking the Golgi to the actin cytoskeleton.
Binding of the extreme carboxyl-terminus of PAK-interacting exchange factor β (βPIX) to myosin 18A (MYO18A) is required for epithelial cell migration.
Yu et al., Taiwan. In Biochim Biophys Acta, 2014
Further experiments using deletion mutants of MYO18A and βPIX showed that disruption of MYO18A-βPIX interaction not only impaired cell motility but also decreased Rac1 activity.
Adaptor protein LRAP25 mediates myotonic dystrophy kinase-related Cdc42-binding kinase (MRCK) regulation of LIMK1 protein in lamellipodial F-actin dynamics.
Tan et al., Singapore, Singapore. In J Biol Chem, 2014
Myotonic dystrophy kinase-related Cdc42-binding kinase (MRCK) has been shown to localize to the lamella of mammalian cells through its interaction with an adaptor protein, leucine repeat adaptor protein 35a (LRAP35a), which links it with myosin 18A (MYO18A) for activation of the lamellar actomyosin network essential for cell migration.
The PDZ-containing unconventional myosin XVIIIA regulates embryonic muscle integrity in zebrafish.
Shi et al., Jinan, China. In J Genet Genomics, 2014
Myosin XVIIIA, or MYO18A, is a unique PDZ domain-containing unconventional myosin and is evolutionarily conserved from Drosophila to vertebrates.
DNA damage triggers Golgi dispersal via DNA-PK and GOLPH3.
Field et al., San Diego, United States. In Cell, 2014
We further show that DNA-damage-induced Golgi dispersal requires GOLPH3/MYO18A/F-actin and the DNA damage protein kinase, DNA-PK.
GOLPH3L antagonizes GOLPH3 to determine Golgi morphology.
Field et al., San Diego, United States. In Mol Biol Cell, 2013
GOLPH3 does so through its ability to link trans-Golgi membranes to F-actin via its interaction with myosin 18A (MYO18A).
Assessing current therapeutic approaches to decode potential resistance mechanisms in glioblastomas.
Chang et al., Tainan City, Taiwan. In Front Oncol, 2012
The potential role of TIAF1 (TGF-β-induced antiapoptotic factor) overexpression and generation of intratumor amyloid fibrils for conferring drug resistance in GBMs is discussed.
Role of phosphatidylinositol 4-phosphate (PI4P) and its binding protein GOLPH3 in hepatitis C virus secretion.
Siddiqui et al., San Diego, United States. In J Biol Chem, 2012
GOLPH3 is shown to maintain a tensile force on the Golgi, required for vesicle budding via its interaction with an unconventional myosin, MYO18A.
Survivin selective inhibitor YM155 induce apoptosis in SK-NEP-1 Wilms tumor cells.
Pan et al., Suzhou, China. In Bmc Cancer, 2011
IPA analysis also showed top molecules up-regulated were BBC3, BIRC3, BIRC8, BNIP1, CASP7, CASP9, CD5, CDKN1A, CEBPG and COL4A3, top molecules down-regulated were ZNF443, UTP11L, TP73, TNFSF10, TNFRSF1B, TNFRSF25, TIAF1, STK17A, SST and SPP1, upstream regulator were NR3C1, TP53, dexamethasone , TNF and Akt.
TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in p53-deficient environment, and cell death.
Chang et al., Tainan City, Taiwan. In Cell Death Dis, 2011
In vitro induction of TIAF1 self-association upregulated the expression of tumor suppressors Smad4 and WW domain-containing oxidoreductase (WOX1 or WWOX), and WOX1 in turn increased the TIAF1 expression.
Proteomics analysis of the ezrin interactome in B cells reveals a novel association with Myo18aα.
Gupta et al., Cleveland, United States. In J Proteome Res, 2011
Myo18aalpha as a novel binding partner of ezrin; the Myo18aalpha/ezrin complex may facilitate B cell receptor-mediated signaling
Identification of MYO18A as a novel interacting partner of the PAK2/betaPIX/GIT1 complex and its potential function in modulating epithelial cell migration.
Yu et al., Didao, China. In Mol Biol Cell, 2010
MYO18A is a novel binding partner of the PAK2/betaPIX/GIT1 complex and suggest that MYO18A may play an important role in regulating epithelial cell migration via affecting multiple cell machineries.
TGF-β induces TIAF1 self-aggregation via type II receptor-independent signaling that leads to generation of amyloid β plaques in Alzheimer's disease.
Chang et al., Taiwan. In Cell Death Dis, 2009
TIAF1 undergoes self-aggregation in response to TGF-Beta1.
Pulmonary surfactant: an immunological perspective.
Shepherd et al., Tyler, United States. In Cell Physiol Biochem, 2009
Several receptors (SP-R210, CD91/calreticulin, SIRPalpha, and toll-like receptors) mediate the immunological functions of SP-A and SP-D.
GOLPH3 bridges phosphatidylinositol-4- phosphate and actomyosin to stretch and shape the Golgi to promote budding.
Field et al., San Diego, United States. In Cell, 2009
GOLPH3 bridges phosphatidylinositol-4- phosphate and actomyosin (via MYO18A) to stretch and shape the Golgi to promote budding.
A tripartite complex containing MRCK modulates lamellar actomyosin retrograde flow.
Leung et al., Singapore, Singapore. In Cell, 2008
We report that the Rac/Cdc42-binding kinase MRCK and myosin II-related MYO18A linked by the adaptor protein LRAP35a form a functional tripartite complex, which is responsible for the assembly of lamellar actomyosin bundles and of a subnuclear actomyosin network.
Pulmonary collectins in innate immunity of the lung.
Nishitani et al., Sapporo, Japan. In Cell Microbiol, 2007
SP-A serves as an opsonin and stimulates the uptake of bacteria and bacillus Calmette-Guérin through a C1q receptor- and an SP-R210-mediated processes.
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