Ask about this productRelated genes to: CSTF1 antibody
- Gene:
- CSTF1 NIH gene
- Name:
- cleavage stimulation factor subunit 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20q13.2-q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-12
- Date modifiied:
- 2018-02-13
Related products to: CSTF1 antibody
Related articles to: CSTF1 antibody
- Hepatocellular carcinoma (HCC) is a aggressive cancer associated with high morbidity and mortality globally. Reliable biomarkers are urgently needed to enhance diagnostic accuracy and survival outcomes in patients with HCC. This study aimed to evaluate the prognostic value of cleavage stimulation factor subunit 1 (CSTF1) in HCC. - Source: PubMed
Publication date: 2025/12/11
Aimaiti MaimaitimingMaimaitituxun DilimulatiYilihaer XiaokaitiKuerban TalifujiangZhu JunlingAiniwaer MieradilijiangJia ZhiqiangAbudourousuli Ainiwaerjiang - Genome-wide association studies (GWASs) in Alzheimer disease (AD) have uncovered over 70 loci significantly associated with AD risk, but identifying the true causal gene(s) at these loci requires systematic functional validation that is rarely performed due to limitations of time and cost. Here, we integrate transcriptome-wide association study (TWAS) with colocalization analysis, fine-mapping, and additional annotation of AD GWAS variants to identify 123 genes at known and suggestive AD risk loci. A comparison with human AD brain transcriptome data confirmed that many of these candidate genes are dysregulated in human AD and correlate with neuropathology. We then tested all available orthologs in two well-established Drosophila AD models that express either wild-type tau or secreted β-amyloid (β42). Experimental perturbation of the 60 available candidates pinpointed 46 that modulated neuronal dysfunction in one or both fly models. The effects of 18 of these genes were concordant with the TWAS prediction, such that the direction of misexpression predicted to increase AD risk in humans exacerbated behavioral impairments in the AD fly models. Reversing the aberrant down- or upregulation of 11 of these genes (MTCH2, ELL, TAP2, HDC, DMWD, MYCL, SLC4A9, ABCA7, CSTF1, PTK2B, and CD2AP) proved neuroprotective in vivo. We further studied MTCH2 and found that it regulates steady-state tau protein levels in the Drosophila brain and reduces tau accumulation in human neural progenitor cells. This systematic, integrative approach effectively prioritizes genes at GWAS loci and reveals promising AD-relevant candidates for further investigation as risk factors or targets for therapeutic intervention. - Source: PubMed
Publication date: 2025/04/10
Stephens Morgan CLi JiayangMair MeganMoore JustinZhu KatyTarkunde AkashAmoh BismarkPerez Alma MBhakare AryaGuo FangfeiShulman Joshua MAl-Ramahi IsmaelBotas Juan - The vast majority of gastrointestinal stromal tumors (GISTs) are driven by activating mutations in , , or components of the succinate dehydrogenase (SDH) complex (, , , and genes). A small fraction of GISTs lack alterations in , , and . We aimed to further characterize the clinical and genomic characteristics of these so-called "triple-negative" GISTs. We extracted clinical and genomic data from patients seen at MD Anderson Cancer Center with a diagnosis of GIST and available clinical next generation sequencing data to identify "triple-negative" patients. Of the 20 patients identified, 11 (55.0%) had gastric, 8 (40.0%) had small intestinal, and 1 (5.0%) had rectal primary sites. In total, 18 patients (90.0%) eventually developed recurrent or metastatic disease, and 8 of these presented with de novo metastatic disease. For the 13 patients with evaluable response to imatinib (e.g., neoadjuvant treatment or for recurrent/metastatic disease), the median PFS with imatinib was 4.4 months (range 0.5-191.8 months). Outcomes varied widely, as some patients rapidly developed progressive disease while others had more indolent disease. Regarding potential genomic drivers, four patients were found to have alterations in the RAS/RAF/MAPK pathway: two with a V600E mutation and two with loss-of-function (LOF) mutations (one deletion and one splice site mutation). In addition, we identified two with LOF mutations, one with fusion (), one with deletion, one with gain-of-function (GOF) mutation (K654E), one with LOF mutation (T367fs*), one with Aurora kinase A fusion (), and one with deletion. Patients had better responses with molecularly targeted therapies than with imatinib. Triple-negative GISTs comprise a diverse cohort with different driver mutations. Compared to /-mutant GIST, limited benefit was observed with imatinib in triple-negative GIST. In depth molecular profiling can be helpful in identifying driver mutations and guiding therapy. - Source: PubMed
Publication date: 2024/04/27
Denu Ryan AJoseph Cissimol PUrquiola Elizabeth SByrd Precious SYang Richard KRatan RavinZarzour Maria AlejandraConley Anthony PAraujo Dejka MRavi VinodNassif Haddad Elise FNakazawa Michael SPatel ShreyaskumarWang Wei-LienLazar Alexander JSomaiah Neeta - Alzheimer's disease (AD) is a genetic and sporadic neurodegenerative disease considered by an archetypal cognitive impairment and a decrease in less common cognitive impairment. Notably, the discovery of goals in this paradigm is still a challenge, and understanding basic mechanisms is an important step toward improving disease management. Polyadenylation (PA) and alternative polyadenylation (APA) are two of the most critical RNA processing stages in 3'UTRs that influence various AD-related genes. - Source: PubMed
Publication date: 2023/11/21
Yeganeh Markid TarlanHosseinpour Feizi Mohammad AliTalebi MahnazRezazadeh MaryamKhalaj-Kondori Mohammad - The aim of the study was to explore the potential molecular mechanism associated with shear stress on abdominal aortic aneurysm (AAA) progression. This study performed RNA sequencing on AAA patients (SQ), AAA patients after endovascular aneurysm repair (EVAR, SH), and normal controls (NC). Furthermore, we identified the differentially expressed microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNA (cirRNAs) and constructed competing endogenous RNA (ceRNA) networks. Finally, 164 differentially expressed miRNAs, 179 co-differentially expressed lncRNAs, and 440 co-differentially expressed circRNAs among the three groups were obtained. The differentially expressed miRNAs mainly enriched in 325 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Target genes associated with co-differentially expressed genes among the group of SH, SQ, and NC mainly enriched in 66 KEGG pathways. LncRNA-miRNA-mRNA interactions, including 15 lncRNAs, 63 miRNAs and 57 mRNAs, was constructed. CircRNA-miRNA-mRNA ceRNA network included 79 circRNAs, 21 miRNAs, and 49 mRNAs. Among them, KLRC2 and CSTF1, targeted by miR-125b, participated in cell-mediated immunity regulation. MiR-320-related circRNAs and SATB1-AS1 serving as the sponge of miRNAs, such as has-circ-0129245, has-circ-0138746, and has-circ-0139786, were hub genes in ceRNA network. In conclusion, AAA patients might be benefit from EVAR based on various pathways and some molecules, such as miR-125b and SATB1-AS1, related with shear stress. - Source: PubMed
Publication date: 2023/01/06
Li Guo-JianYang Qiong-HuiYang Guo-KaiYang GuangHou YiHou Li-JuanLi Zhao-XiangDu Ling-Juan