| SP-R210 isoforms of Myosin18A modulate endosomal sorting and recognition of influenza A virus infection in macrophages. | SP-R210 isoforms of Myosin18A modulate endosomal sorting and recognition of influenza A virus infection in macrophages.
Yau E, Yang L, Chen Y, Umstead TM, Stanley AE, Halstead ES, Gandhi CK, Yewdell JW, Chroneos ZC., | 03/20/2024 |
| Expression of TIAF-1 in the lymphocytes during chronic allograft rejection may be related to the predominance of a Th2 response in this condition and may protect these cells from apoptosis | High expression of TIAF-1 in chronic kidney and liver allograft rejection and in activated T-helper cells.
van der Leij J, van den Berg A, Albrecht EW, Blokzijl T, Roozendaal R, Gouw AS, de Jong KP, Stegeman CA, van Goor H, Chang NS, Poppema S. | 01/15/2022 |
| TIAF1 and p53 functionally interact in regulating apoptosis, and TIAF1 is likely to participate in the nuclear translocation of activated p53. | TIAF1 and p53 functionally interact in mediating apoptosis and silencing of TIAF1 abolishes nuclear translocation of serine 15-phosphorylated p53.
Schultz L, Khera S, Sleve D, Heath J, Chang NS. | 01/15/2022 |
| 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. | TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in p53-deficient environment, and cell death.
Chang JY, Chiang MF, Lin SR, Lee MH, He H, Chou PY, Chen SJ, Chen YA, Yang LY, Lai FJ, Hsieh CC, Hsieh TH, Sheu HM, Sze CI, Chang NS., Free PMC Article | 01/15/2022 |
| TIAF1 undergoes self-aggregation in response to TGF-Beta1. | TGF-β induces TIAF1 self-aggregation via type II receptor-independent signaling that leads to generation of amyloid β plaques in Alzheimer's disease.
Lee MH, Lin SR, Chang JY, Schultz L, Heath J, Hsu LJ, Kuo YM, Hong Q, Chiang MF, Gong CX, Sze CI, Chang NS., Free PMC Article | 01/15/2022 |
| a high proportion of MYO18A is found in complex with GOLPH3 at the trans Golgi, where it functions to promote vesicle budding for Golgi-to-plasma membrane trafficking. | MYO18A: An unusual myosin.
Buschman MD, Field SJ., Free PMC Article | 09/14/2019 |
| Studies indicate that MYO18A is overexpressed in metastatic prostate cancer (PC-3) cells. | How myosin organization of the actin cytoskeleton contributes to the cancer phenotype.
Peckham M. | 07/15/2017 |
| Identification of the DNA-damage-induced Golgi response reveals an unexpected pathway through DNA-PK, GOLPH3, and MYO18A that regulates cell survival following DNA damage. | DNA damage triggers Golgi dispersal via DNA-PK and GOLPH3.
Farber-Katz SE, Dippold HC, Buschman MD, Peterman MC, Xing M, Noakes CJ, Tat J, Ng MM, Rahajeng J, Cowan DM, Fuchs GJ, Zhou H, Field SJ., Free PMC Article | 04/26/2014 |
| PDZ module mediates direct binding of myosin-18A to GOLPH3, and this interaction in turn modulates the actin binding properties of the N-terminal extension. Thus, myosin-18A can act as an actin cross-linker with multiple regulatory modulators | Functional characterization of human myosin-18A and its interaction with F-actin and GOLPH3.
Taft MH, Behrmann E, Munske-Weidemann LC, Thiel C, Raunser S, Manstein DJ., Free PMC Article | 01/4/2014 |
| GOLPH3L differs critically from GOLPH3 in that it is largely unable to bind to MYO18A; data demonstrate that despite their similarities, unexpectedly, GOLPH3L antagonizes GOLPH3/MYO18A at the Golgi | GOLPH3L antagonizes GOLPH3 to determine Golgi morphology.
Ng MM, Dippold HC, Buschman MD, Noakes CJ, Field SJ., Free PMC Article | 09/14/2013 |
| Myo18aalpha as a novel binding partner of ezrin; the Myo18aalpha/ezrin complex may facilitate B cell receptor-mediated signaling | Proteomics analysis of the ezrin interactome in B cells reveals a novel association with Myo18aα.
Matsui K, Parameswaran N, Bagheri N, Willard B, Gupta N., Free PMC Article | 03/3/2012 |
| GOLPH3 bridges phosphatidylinositol-4- phosphate and actomyosin (via MYO18A) to stretch and shape the Golgi to promote budding. | GOLPH3 bridges phosphatidylinositol-4- phosphate and actomyosin to stretch and shape the Golgi to promote budding.
Dippold HC, Ng MM, Farber-Katz SE, Lee SK, Kerr ML, Peterman MC, Sim R, Wiharto PA, Galbraith KA, Madhavarapu S, Fuchs GJ, Meerloo T, Farquhar MG, Zhou H, Field SJ., Free PMC Article | 03/2/2011 |
| Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator) | Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score.
Rose JE, Behm FM, Drgon T, Johnson C, Uhl GR., Free PMC Article | 06/30/2010 |
| 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. | Identification of MYO18A as a novel interacting partner of the PAK2/betaPIX/GIT1 complex and its potential function in modulating epithelial cell migration.
Hsu RM, Tsai MH, Hsieh YJ, Lyu PC, Yu JS., Free PMC Article | 03/29/2010 |
| These findings support the hypothesis that SP-A, via SP-R210, suppresses cell-mediated immunity against M. tuberculosis via a mechanism that up-regulates secretion of IL-10 and TGF-beta1.[SP-A receptor] | An antibody against the surfactant protein A (SP-A)-binding domain of the SP-A receptor inhibits T cell-mediated immune responses to Mycobacterium tuberculosis.
Samten B, Townsend JC, Sever-Chroneos Z, Pasquinelli V, Barnes PF, Chroneos ZC., Free PMC Article | 01/21/2010 |
| Study used a DNA-based long-distance inverse PCR (LDI-PCR) to identify a new MYO18A-PDGFRB fusion gene in an Eos-MPN (eosinophilia-associated atypical myeloproliferative neoplasms) with associated t(5;17)(q33-34;q11.2). | Identification of a MYO18A-PDGFRB fusion gene in an eosinophilia-associated atypical myeloproliferative neoplasm with a t(5;17)(q33-34;q11.2).
Walz C, Haferlach C, Hänel A, Metzgeroth G, Erben P, Gosenca D, Hochhaus A, Cross NC, Reiter A. | 01/21/2010 |
| this dimeric myosin might stably cross-link actin filaments by two ATP-insensitive actin-binding sites at the N-terminal domains for higher-order organization of the actin cytoskeleton | The N-terminal domain of MYO18A has an ATP-insensitive actin-binding site.
Isogawa Y, Kon T, Inoue T, Ohkura R, Yamakawa H, Ohara O, Sutoh K. | 01/21/2010 |
| MyoXVIIIA constitutes a novel receptor for SP-A | Identification of the surfactant protein A receptor 210 as the unconventional myosin 18A.
Yang CH, Szeliga J, Jordan J, Faske S, Sever-Chroneos Z, Dorsett B, Christian RE, Settlage RE, Shabanowitz J, Hunt DF, Whitsett JA, Chroneos ZC., Free PMC Article | 01/21/2010 |