Ask about this productRelated genes to: SLFNL1 antibody
- Gene:
- SLFNL1 NIH gene
- Name:
- schlafen like 1
- Previous symbol:
- -
- Synonyms:
- FLJ23878
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-04-05
- Date modifiied:
- 2015-11-11
Related products to: SLFNL1 antibody
Related articles to: SLFNL1 antibody
- Androgen deprivation therapy (ADT) is the primary treatment strategy for prostate cancer. However, despite an initially favorable response, tumors inevitably progress to castration-resistant prostate cancer (CRPC). Therefore, the exploration of new therapeutic approaches targeting CRPC has become imperative. Increasing evidence suggests that hypoxia plays a crucial role in the development of CRPC. In this study, we found that the emergence of alkaliptosis resistance and the expression of its marker, CA9, significantly contribute to the progression of castration resistance induced by hypoxia. This study utilized bioinformatics approaches to identify genetic determinants associated with alkaliptosis resistance and explored the clinical significance of these marker genes. Transcriptomic sequencing was performed on the DU145 prostate cancer cell line, which had been induced to acquire alkaliptosis resistance. Using least absolute shrinkage and selection operator (LASSO) regression analysis, a prognostic risk model consisting of 12 genes, including ADORA2A, KCNG4, SEC14L5, B3GAT2, SLFNL1, FAM72D, CBWD3, PPM1K, STARD4, DEPDC1B, MATN3, and DDIAS was developed. The risk model score demonstrated a strong correlation with key patient clinical characteristics, including Gleason score, PSA levels, T stage, and N stage, and was also associated with immune therapy response and biochemical recurrence-free survival (BCRFS). Furthermore, ADORA2A expression in cellular models was found to be a critical factor in promoting alkaliptosis resistance. - Source: PubMed
Publication date: 2025/01/06
Song XiaodongZhang YuLi TiewenWang WenhaoXie ZhiwenHan Bangmin - Chronic obstructive pulmonary disease (COPD) is a common chronic disease of the respiratory tract, with high prevalence, high disability, and poor prognosis. However, the molecular mechanism of COPD needs to be further revealed. - Source: PubMed
Publication date: 2022/10/04
Han HuiHao Lu - We aim to identify the expression and analyze the molecular action of dysregulated lncRNA-miRNA mediated by XBP-1 in colorectal cancer (CRC). - Source: PubMed
Publication date: 2021/09/14
Wang YongZhang JingyuZheng Shuang - As the world population continues to increase to unsustainable levels, the importance of birth control and the development of new contraceptives are emerging. To date, male contraceptive options have been lagging behind those available to women, and those few options available are not satisfactory to everyone. To solve this problem, we have been searching for new candidate target proteins for non-hormonal contraceptives. Testis-specific proteins are appealing targets for male contraceptives because they are more likely to be involved in male reproduction and their targeting by small molecules is predicted to have no on-target harmful effects on other organs. Using in silico analysis, we identified Erich2, Glt6d1, Prss58, Slfnl1, Sppl2c, Stpg3, Tex33, and Tex36 as testis-abundant genes in both mouse and human. The genes, 4930402F06Rik and 4930568D16Rik, are testis-abundant paralogs of Glt6d1 that we also discovered in mice but not in human, and were also included in our studies to eliminate the potential compensation. We generated knockout (KO) mouse lines of all listed genes using the CRISPR/Cas9 system. Analysis of all of the individual KO mouse lines as well as Glt6d1/4930402F06Rik/4930568D16Rik TKO mouse lines revealed that they are male fertile with no observable defects in reproductive organs, suggesting that these 10 genes are not required for male fertility nor play redundant roles in the case of the 3 Glt6D1 paralogs. Further studies are needed to uncover protein function(s), but in vivo functional screening using the CRISPR/Cas9 system is a fast and accurate way to find genes essential for male fertility, which may apply to studies of genes expressed elsewhere. In this study, although we could not find any potential protein targets for non-hormonal male contraceptives, our findings help to streamline efforts to find and focus on only the essential genes. - Source: PubMed
Park SoojinShimada KeisukeFujihara YoshitakaXu ZoulanShimada KentaroLarasati TamaraPratiwi PutriMatzuk Ryan MDevlin Darius JYu ZhifengGarcia Thomas XMatzuk Martin MIkawa Masahito - Endothelial progenitor cells (EPCs) are the major source of cells that restore the endothelium during reendothelialization. This study was designed to investigate whether Schlafen 1 (Slfn1) has an effect on the proliferation and tube formation of EPCs in vivo. Slfn1 was expressed in rat EPCs. The overexpression of Slfn1 suppressed the proliferation and tube formation of EPCs; conversely, the knockdown of Slfn1 by shRNA promoted the proliferation and tube formation of EPCs. Furthermore, when Slfn1 was overexpressed, the EPCs were arrested in the G1 phase of the cell cycle. In contrast, when Slfn1 was knocked down, the EPCs progressed into the S phase of the cell cycle. Additionally, the overexpression of Slfn1 decreased the expression of Cyclin D1, whereas the knockdown of Slfn1 increased the expression of Cyclin D1; these findings suggest that Cyclin D1 is downstream of Slfn1 in Slfn1-mediated EPC proliferation. Taken together, these results indicate a key role for Slfn1 in the regulation of EPC biological behavior, which may provide a new target for the use of EPCs during reendothelialization. - Source: PubMed
Publication date: 2014/10/16
Kuang Chun-yanYang Tian-heZhang YangZhang LuWu Qiang