| Myosin18B predicts favorable prognosis of cutaneous squamous-cell carcinoma. | Myosin18B predicts favorable prognosis of cutaneous squamous-cell carcinoma.
Cao C, Zhang C, Sun Y, Mu Z, Shen Q. | 01/29/2022 |
| Further delineation of MYO18B-related autosomal recessive Klippel-Feil syndrome with myopathy and facial dysmorphism. | Further delineation of MYO18B-related autosomal recessive Klippel-Feil syndrome with myopathy and facial dysmorphism.
Altuame FD, Haldeman-Englert C, Cupler E, Al Muhaizea MA, Al-Zaidan HI, Hashem M, Alkuraya FS. | 07/10/2021 |
| Myosin-18B Regulates Higher-Order Organization of the Cardiac Sarcomere through Thin Filament Cross-Linking and Thick Filament Dynamics. | Myosin-18B Regulates Higher-Order Organization of the Cardiac Sarcomere through Thin Filament Cross-Linking and Thick Filament Dynamics.
Latham SL, Weiß N, Schwanke K, Thiel C, Croucher DR, Zweigerdt R, Manstein DJ, Taft MH. | 05/29/2021 |
| The results reveal a critical role for myosin-18B in myosin II stack assembly and provide evidence that myosin II stacks are important for a variety of vital processes in cells. | Myosin-18B Promotes the Assembly of Myosin II Stacks for Maturation of Contractile Actomyosin Bundles.
Jiu Y, Kumari R, Fenix AM, Schaible N, Liu X, Varjosalo M, Krishnan R, Burnette DT, Lappalainen P., Free PMC Article | 01/25/2020 |
| MYO18B promoted hepatocellular carcinoma growth and migration via the activation of PI3K/AKT/mTOR signaling pathway. | MYO18B promotes hepatocellular carcinoma progression by activating PI3K/AKT/mTOR signaling pathway.
Zhang Z, Zhu J, Huang Y, Li W, Cheng H., Free PMC Article | 03/16/2019 |
| Full loss of myo18b function results in a complete lack of sarcomeric structure, revealing a highly surprising and essential role for myo18b in sarcomere assembly. Importantly, scattered thin and thick filaments assemble throughout the sarcoplasm. These observations suggest a novel model of sarcomere assembly where Myo18b coordinates the integration of preformed thick and thin filaments into the sarcomere | Myo18b is essential for sarcomere assembly in fast skeletal muscle.
Berger J, Berger S, Li M, Currie PD. | 05/20/2017 |
| Deficiency of MYO18B is linked to a novel developmental disorder which combines KFA with myopathy. | A novel syndrome of Klippel-Feil anomaly, myopathy, and characteristic facies is linked to a null mutation in MYO18B.
Alazami AM, Kentab AY, Faqeih E, Mohamed JY, Alkhalidi H, Hijazi H, Alkuraya FS. | 02/27/2016 |
| No associations were found between rs133885 in myosin-18B and mathematical abilities among individuals with dyslexia or in the general population. | Lack of replication for the myosin-18B association with mathematical ability in independent cohorts.
Pettigrew KA, Fajutrao Valles SF, Moll K, Northstone K, Ring S, Pennell C, Wang C, Leavett R, Hayiou-Thomas ME, Thompson P, Simpson NH, Fisher SE, SLI Consortium, Whitehouse AJ, Snowling MJ, Newbury DF, Paracchini S., Free PMC Article | 01/23/2016 |
| A common MYO18B variant is associated with mathematical disability in children with dyslexia and with intraparietal sulcus variability in neurotypical adults. | A common variant in myosin-18B contributes to mathematical abilities in children with dyslexia and intraparietal sulcus variability in adults.
Ludwig KU, Sämann P, Alexander M, Becker J, Bruder J, Moll K, Spieler D, Czisch M, Warnke A, Docherty SJ, Davis OS, Plomin R, Nöthen MM, Landerl K, Müller-Myhsok B, Hoffmann P, Schumacher J, Schulte-Körne G, Czamara D., Free PMC Article | 08/31/2013 |
| 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 |
| Clinical trial and genome-wide association study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator) | Molecular genetics of successful smoking cessation: convergent genome-wide association study results.
Uhl GR, Liu QR, Drgon T, Johnson C, Walther D, Rose JE, David SP, Niaura R, Lerman C., Free PMC Article | 12/2/2009 |
| The restored expression of MYO18B may be a useful therapeutic strategy for the treatment of locally advanced Malignant pleural mesothelioma(MPM)in humans. | Restored expression of the MYO18B gene suppresses orthotopic growth and the production of bloody pleural effusion by human malignant pleural mesothelioma cells in SCID mice.
Edakuni N, Ikuta K, Yano S, Nakataki E, Muguruma H, Uehara H, Tani M, Yokota J, Aizawa H, Sone S. | 01/21/2010 |
| MYO18B alterations, including both epigenetic and genetic alterations, play an important role in ovarian carcinogenesis | Reduced expression of MYO18B, a candidate tumor-suppressor gene on chromosome arm 22q, in ovarian cancer.
Yanaihara N, Nishioka M, Kohno T, Otsuka A, Okamoto A, Ochiai K, Tanaka T, Yokota J. | 01/21/2010 |
| Human MYO18B, a novel unconventional myosin heavy chain expressed in striated muscles moves into the myonuclei upon differentiation | Human MYO18B, a novel unconventional myosin heavy chain expressed in striated muscles moves into the myonuclei upon differentiation.
Salamon M, Millino C, Raffaello A, Mongillo M, Sandri C, Bean C, Negrisolo E, Pallavicini A, Valle G, Zaccolo M, Schiaffino S, Lanfranchi G. | 01/21/2010 |
| candidate tumor suppressor gene at chromosome 22q12.1, deleted, mutated, and methylated in human lung cancer | MYO18B, a candidate tumor suppressor gene at chromosome 22q12.1, deleted, mutated, and methylated in human lung cancer.
Nishioka M, Kohno T, Tani M, Yanaihara N, Tomizawa Y, Otsuka A, Sasaki S, Kobayashi K, Niki T, Maeshima A, Sekido Y, Minna JD, Sone S, Yokota J., Free PMC Article | 01/21/2010 |
| Proteasome dysfunction by a proteasome inhibitor or siRNA-mediated knock-down of Sug1 caused the up-regulation of MYO18B protein and MYO18B was polyubiquitinated in vivo. | MYO18B interacts with the proteasomal subunit Sug1 and is degraded by the ubiquitin-proteasome pathway.
Inoue T, Kon T, Ajima R, Ohkura R, Tani M, Yokota J, Sutoh K. | 01/21/2010 |