RASL11B is a member of the small GTPase protein family with a high degree of similarity to RAS proteins. Cloning of RASL11B mRNA and in silico analyses revealed that the human RASL11B gene spans about 4.5 kb and comprises four exons on chromosomal locus 4q12. The proximal 5'-flanking region of the gene lacks a TATA box but is GC-rich and contains a CCAAT box and several Sp1 sites. Consistent with this, the RASL11B gene was found to be expressed in all tissues investigated, with highest levels in placenta and in primary macrophages. The predicted RASL11B protein has no typical prenylation signal, indicating that it is probably not anchored to cellular membranes. RASL11B was induced during maturation of THP-1 monocytic cells into macrophage-like cells and in coronary artery smooth muscle cells after treatment with TGF-beta1. These results indicate that RASL11B may play a role in TGF-beta1-mediated developmental processes and in pathophysiologies such as inflammation, cancer, and arteriosclerosis.
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http://dx.doi.org/10.1016/j.bbaexp.2007.05.005 | DOI Listing |
PLoS One
October 2023
Department of Biology, University of York, Heslington, York, United Kingdom.
Activation of Map kinase/Erk signalling downstream of fibroblast growth factor (Fgf) tyrosine kinase receptors regulates gene expression required for mesoderm induction and patterning of the anteroposterior axis during Xenopus development. We have proposed that a subset of Fgf target genes are activated in the embyo in response to inhibition of a transcriptional repressor. Here we investigate the hypothesis that Cic (Capicua), which was originally identified as a transcriptional repressor negatively regulated by receptor tyrosine kinase/Erk signalling in Drosophila, is involved in regulating Fgf target gene expression in Xenopus.
View Article and Find Full Text PDFBMC Res Notes
October 2023
Department of Animal Science, University of California Davis, 2251 Meyer Hall, One Shields Ave, Davis, CA, 95616, USA.
Objectives: Equine tendinopathies are challenging because of the poor healing capacity of tendons commonly resulting in high re-injury rates. Within the tendon, different regions - tendon proper (TP) and peritenon (PERI) - contribute to the tendon matrix in differing capacities during injury and aging. Aged tendons have decreased repair potential; the underlying transcriptional and epigenetic changes that occur in the TP and PERI regions are not well understood.
View Article and Find Full Text PDFJ Invest Dermatol
July 2023
National Center for Tumor Diseases (NCT/UCC), Dresden, Germany: German Cancer Research Center (DKFZ), Heidelberg, Germany; Medizinische Fakultät and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany; Helmholtz-Zentrum Dresden - Rossendorf (HZDR), Dresden, Germany; Institute for Medical Informatics and Biometry, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Despite remarkable advances in treating patients with metastatic melanoma, the management of melanoma brain metastases remains challenging. Recent evidence suggests that epigenetic reprogramming is an important mechanism for the adaptation of melanoma cells to the brain environment. In this study, the methylomes and transcriptomes of a cohort of matched melanoma metastases were evaluated by integrated omics data analysis.
View Article and Find Full Text PDFBiochem Cell Biol
August 2021
Department of Anesthesiology, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Numerous studies have indicated that microRNAs (miRNAs) play critical roles in the development and progression of cancer. However, how changes to the expression levels of miRNAs in response to dexmedetomidine affects the progression of lung cancer remains poorly understood. In this study, we treated the lung adenocarcinoma cell line-A549 with dexmedetomidine and then examined the changes to the expression levels of miRNAs.
View Article and Find Full Text PDFBMC Cancer
May 2021
Department of Urology, First hospital of China Medical University, Shenyang, Liaoning, China.
Background: The tumour microenvironment (TME) not only plays a role during tumour progression and metastasis but also profoundly influences treatment efficacy. Environment-mediated drug resistance is a result of crosstalk between tumour cells and stroma. The presence of a "stromal exhaustion" response is suggested by the T cell exhaustion signature and PD-L1 expression.
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