Ask about this productRelated genes to: RASL10A Blocking Peptide
- Gene:
- RASL10A NIH gene
- Name:
- RAS like family 10 member A
- Previous symbol:
- -
- Synonyms:
- RRP22
- Chromosome:
- 22q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-01-15
- Date modifiied:
- 2016-02-01
Related products to: RASL10A Blocking Peptide
Related articles to: RASL10A Blocking Peptide
- Lung adenocarcinoma (LUAD) is the most frequently diagnosed form of non-small cell lung cancer and is known to develop distant metastases, such as brain and bone metastases, which can considerably affect the prognosis of patients. Therefore, there is a need to elucidate the metastatic mechanisms of LUAD and establish treatments to control metastasis. In this study, Kaplan-Meier plotter analysis demonstrated that patients with LUAD and low RASL10A expression have a poor prognosis. Furthermore, loss or gain of function experiments revealed that RASL10A suppresses transforming growth factor-beta (TGF-β)-induced epithelial-mesenchymal transition (EMT) and the subsequent invasion of LUAD A549 cells. In addition, we found that RASL10A suppresses Smad3 phosphorylation and Snail expression during the early stages of EMT. These results indicate that RASL10A is a novel factor that inhibits TGF-β signaling-mediated EMT and invasion in A549 cells. RASL10A has the potential to become a new therapeutic target for patients with LUAD. - Source: PubMed
Nishizuka MakotoNakajima KanaeOdagiri ChieWada NanakaSakai Satoshi - The small GTPase family is well-studied in cancer and cellular physiology. With 162 annotated human genes, the family has a broad expression throughout cells of the body. Members of the family have multiple exons that require splicing. Yet, the role of splicing within the family has been underexplored. We have studied the splicing dynamics of small GTPases throughout 41,671 samples by integrating Nanopore and Illumina sequencing techniques. Within this work, we have made several discoveries. 1). Using the GTEx long read data of 92 samples, each small GTPase gene averages two transcripts, with 83 genes (51%) expressing two or more isoforms. 2). Cross-tissue analysis of GTEx from 17,382 samples shows 41 genes (25%) expressing two or more protein-coding isoforms. These include protein-changing transcripts in genes such as , , , , , , , , , , and . 3). The isolation and library technique of the RNAseq influences the abundance of non-sense-mediated decay and retained intron transcripts of small GTPases, which are observed more often in genes than appreciated. 4). Analysis of 16,243 samples of "Blood PAXgene" identified seven genes (3.7%; , , , , , , ) with two or more transcripts expressed as the major isoform (75% of the total gene), suggesting a role of genetics in altering splicing. 5). Rare (, , , , ) and common variants (, , , , , ) can influence splicing and have an impact on phenotypes and diseases. 6). Multiple genes (, , , , , , , , and ) have sex differences in transcript expression. 7). Several exons are included or excluded for small GTPase genes (, , , , , , , , , ) in one or more forms of cancer. 8). Ten transcripts are altered in hypoxia (, , , , , , , , ) with identified to have a transient 3'UTR RNA base editing at a conserved site found in all of its transcripts. Overall, we show a remarkable and dynamic role of splicing within the small GTPase family that requires future explorations. - Source: PubMed
Publication date: 2022/11/17
Das Akansha SSherry Emily CVaughan Robert MHenderson Marian LZieba JacobUhl Katie LKoehn OliviaBupp Caleb PRajasekaran SurenderLi XiaopengChhetri Surya BNissim SaharWilliams Carol LProkop Jeremy W - A long-term opioid use has been associated with hypermethylation of the opioid receptor mu 1 (OPRM1) promoter. Very little is currently known about the early epigenetic response to therapeutic opioids. Here, we examine whether we can detect DNA methylation changes associated with a few days' use of prescribed opioids. Genome-wide DNA methylation was assayed in a cohort of 33 opioid-naïve participants who underwent standard dental surgery followed by opioid self-administration. Saliva samples were collected before surgery (visit 1), and at two postsurgery visits at 2.7 ± 1.5 days (visit 2), and 39 ± 10 days (visit 3) after the discontinuation of opioid analgesics. - Source: PubMed
Publication date: 2020/06/03
Sandoval-Sierra Jose VladimirSalgado García Francisco IBrooks Jeffrey HDerefinko Karen JMozhui Khyobeni - RRP22 (Ras-related protein on chromosome 22) has been suggested as a candidate tumor suppressor in human cancers. Investigating a panel of 70 human gliomas, we found a frequent decrease in the RRP22 mRNA expression levels (67%), preferentially in high-grade gliomas [World Health Organization (WHO) grades III and IV] as compared with low-grade gliomas (WHO grade II). Moreover, reduced RRP22 mRNA expression was associated with shorter overall survival in 180 glioblastoma patients included in the National Institutes of Health Repository for Molecular Brain Neoplasia Data (NIH REMBRANDT) database. Decreased RRP22 expression levels were in part explained by 5'-CpG island hypermethylation and increased by the treatment with the demethylating agent 5-aza-2'-deoxycytidine in glioblastoma cell lines. In addition, the in vitro treatment with the histone deacetylase inhibitor trichostatin A alone resulted in RRP22 reexpression as well as a significant increase in the levels of RRP22 promoter DNA bound to pan-acetylated histone H3 and H4. Moreover, in primary human glioblastomas, we observed an increase of H3K9me3-bound and a decrease of pan-Ac-H3-bound RRP22 in comparison with non-neoplastic brain tissue, consistent with a heterochromatinization of the RRP22 promoter. Taken together, our findings demonstrate that both 5'-CpG island hypermethylation and histone modifications contribute to the frequent and prognostically unfavorable transcriptional downregulation of RRP22 in malignant gliomas. - Source: PubMed
Publication date: 2011/08/16
Schmidt NatalieWindmann SonjaReifenberger GuidoRiemenschneider Markus J - Astrocytomas are the most common neoplasm of the central nervous system. Although progress has been made, the survival rate of astrocytoma is still poor. Therefore, improving the prognosis of patients with astrocytomas relies on effective therapies that are directed against unique molecular aberrations. Previous studies have revealed that a novel member of the Ras superfamily, RRP22, which is located on chromosome 22 on the 12q site, is exclusively expressed in the central nervous system. RRP22 can be modified by farnesyl and down-regulated in a variety of neural tumor cell lines. In this study, we analyzed the mRNA level of RRP22 in normal brain tissues and astrocytomas using quantitative RT-PCR. Our results showed that the mRNA level in astrocytomas was significantly down-regulated compared to levels in normal tissues. As the pathological grade (World Health Organization (WHO) classification 2007) increased, the expression of RRP22 decreased. However, according to our research, there was no significant difference between malignant astrocytomas with pathological grades of III or IV. To investigate the possible effects of RRP22 on the biological behavior of glioma cells, we transfected RRP22 into a malignant cell line of astrocytomas, U251. We found that RRP22 inhibited growth, decreased invasiveness, and induced cell death. Thus, RRP22 is a special neural tumor suppressor for human astrocytomas, although further studies are needed to define the detailed mechanisms. - Source: PubMed
Publication date: 2011/01/25
Chen RuokunYang LiangFang JiashengHuo LeiZhang MingyuChen FenghuaLiu JinfangWu JunWang Yanjin