Ask about this productRelated genes to: SNAPC1 antibody
- Gene:
- SNAPC1 NIH gene
- Name:
- small nuclear RNA activating complex polypeptide 1
- Previous symbol:
- -
- Synonyms:
- SNAP43, PTFgamma
- Chromosome:
- 14q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-12
- Date modifiied:
- 2016-10-05
Related products to: SNAPC1 antibody
Related articles to: SNAPC1 antibody
- The noncoding small nuclear RNAs (snRNAs) associate with a large set of proteins to form small nuclear ribonucleoprotein particles (snRNPs). While the function of snRNAs is well characterized, the regulation of their transcription remains poorly understood. Recently, we demonstrated that SUMO conjugation regulates snRNA3' end processing. To further study the connection between SUMOylation and snRNA biogenesis, we generated a CRISPR/dCas9 tool comprising a catalytically inactive Cas9 (dCas9) fused to the catalytic domain of the SUMO protease SENP1 (dCas9-SENP1). Here, we show that snRNA transcription decreases when dCas9-SENP1 is delivered to their promoter-proximal sequence elements (PSE), indicating that SUMO conjugation to proteins associated with snRNA promoters is necessary for proper transcriptional activity. Focusing on SNAPC1, a subunit of the snRNA-specific transcription complex SNAPc, we identified lysine residues 245 and 333 as SUMO acceptor sites and generated a SUMOylation-deficient mutant of this protein (SNAPC1 2KR). To explore the relevance of SNAPC1 SUMOylation on snRNA transcription, we generated a cell line carrying an inducible degron system for depletion of the endogenous SNAPC1 protein. This system led us to demonstrate that SNAPC1 2KR is unable to sustain basal levels of snRNA transcription. By tagging endogenous SNAPC3 and SNAPC4, two other subunits of SNAPc, we show that while SNAPC1 SUMOylation-deficient mutant is able to interact with SNAPC3, its interaction with SNAPC4 is affected, despite the fact it is still recruited to the PSE. Altogether, these results indicate that SNAPC1 SUMOylation is required for proper snRNA transcription and SNAPc complex assembly. - Source: PubMed
Publication date: 2025/09/16
Bragado LaureanoPozzi BertaBeckerman InésMagalnik MelinaSrebrow Anabella - Acute myeloid leukemia (AML) is a heterogeneous disease and the most common form of acute leukemia with a poor prognosis. Due to its complexity, the disease requires the identification of biomarkers for reliable prognosis. To identify potential disease genes that regulate patient prognosis, we used differential co-expression network analysis and transcriptomics data from relapsed, refractory, and previously untreated AML patients based on their response to treatment in the present study. In addition, we combined functional genomics and transcriptomics data to identify novel and therapeutically potential systems biomarkers for patients who do or do not respond to treatment. As a result, we constructed co-expression networks for response and non-response cases and identified a highly interconnected group of genes consisting of SECISBP2L, MAN1A2, PRPF31, VASP, and SNAPC1 in the response network and a group consisting of PHTF2, SLC11A2, PDLIM5, OTUB1, and KLRD1 in the non-response network, both of which showed high prognostic performance with hazard ratios of 4.12 and 3.66, respectively. Remarkably, ETS1, GATA2, AR, YBX1, and FOXP3 were found to be important transcription factors in both networks. The prognostic indicators reported here could be considered as a resource for identifying tumorigenesis and chemoresistance to farnesyltransferase inhibitor. They could help identify important research directions for the development of new prognostic and therapeutic techniques for AML. - Source: PubMed
Publication date: 2023/12/08
Kelesoglu NurdanKori MediYilmaz Betul KarademirDuru Ozlem AtesArga Kazim Yalcin - To identify and characterize read-through RNAs and read-through circular RNAs (rt-circ-HS) derived from transcriptional read-through hypoxia inducible factor 1α () and small nuclear RNA activating complex polypeptide 1 () the two adjacent genes located on chromosome 14q23, in renal carcinoma cells and renal carcinoma tissues, and to study the effects of rt-circ-HS on biological behavior of renal carcinoma cells and on regulation of . - Source: PubMed
Xu Y YSu Z ZZheng L MZhang M NTan J YYang Y LZhang M XXu MChen NChen X QZhou Q - Chronic stress is one of the key precipitating factors in major depressive disorder (MDD). Stress associated studies have underscored the mechanistic role of epigenetic master players like microRNAs (miRNAs) in depression pathophysiology at both preclinical and clinical levels. Previously, we had reported changes in miR-218-5p expression in response to corticosterone (CORT) induced chronic stress. MiR-218-5p was one of the most significantly induced miRNAs in the prefrontal cortex (PFC) of rats under chronic stress. In the present report, we have investigated how chronic CORT exposure mechanistically affected miR-218-5p expression in the rat brain and how miR-218 could trigger molecular changes on its downstream regulatory pathways. Elevated expression of miR-218-5p was found in the PFC of CORT-treated rats. A glucocorticoid receptor (GR) targeted Chromatin-Immunoprecipitation (ChIP) assay revealed high GR occupancy on the promoter region of Slit3 gene hosting miR-218-2 in its 3rd intron. RNA-sequencing data based on RNA Induced silencing Complex Immunoprecipitation (RISC-IP) with AGO2 in SH-SY5Y cells detected six consistent target genes of miR-218-5p (APOL4, DTWD1, BNIP1, METTL22, SNAPC1, and HDAC6). The expression of all five genes, except APOL4, was successfully validated with qPCR in CORT-treated rat PFC. Further, Hdac6-based ChIP-seq experiment helped in mapping major genomic loci enriched for intergenic regions in the PFC of CORT-treated rat. A proximity-based gene ontology (GO) analysis revealed a majority of the intergenic sites to be part of key genes implicated in central nervous system functions, notably synapse organization, neuron projection morphogenesis, and axonogenesis. Our results suggest that the upregulation of miR-218-5p in PFC of CORT-treated rats possibly resulted from GR biding in the promoter region of Slit3 gene. Interestingly, Hdac6 was one of the consistent target genes potentially found to regulate CNS related genes by chromatin modification. Collectively, these findings establish the role of miR-218-5p in chronic stress and the epigenetic function it plays to induce chromatin-based transcriptional changes of several CNS genes in triggering stress-induced disorders, including depression. This also opens up the scope to understand the role of miR-218-5p as a potential target for noncoding RNA therapeutics in clinical depression. - Source: PubMed
Publication date: 2022/01/07
Yoshino YutaRoy BhaskarDwivedi Yogesh - Identification of genetic factors leading to increased risk of suicide death is critical to combat rising suicide rates, however, only a fraction of the genetic variation influencing risk has been accounted for. To address this limitation, we conducted the first comprehensive analysis of rare genetic variation in suicide death leveraging the largest suicide death biobank, the Utah Suicide Genetic Risk Study (USGRS). We conducted a single-variant association analysis of rare (minor allele frequency <1%) putatively functional single-nucleotide polymorphisms (SNPs) present on the Illumina PsychArray genotyping array in 2,672 USGRS suicide deaths of non-Finnish European (NFE) ancestry and 51,583 NFE controls from the Genome Aggregation Database. Secondary analyses used an independent control sample of 21,324 NFE controls from the Psychiatric Genomics Consortium. Five novel, high-impact, rare SNPs were identified with significant associations with suicide death (SNAPC1, rs75418419; TNKS1BP1, rs143883793; ADGRF5, rs149197213; PER1, rs145053802; and ESS2, rs62223875). 119 suicide decedents carried these high-impact SNPs. Both PER1 and SNAPC1 have other supporting gene-level evidence of suicide risk, and psychiatric associations exist for PER1 (bipolar disorder, schizophrenia), and for TNKS1BP1 and ESS2 (schizophrenia). Three of the genes (PER1, TNKS1BP1, and ADGRF5), together with additional genes implicated by genome-wide association studies on suicidal behavior, showed significant enrichment in immune system, homeostatic and signal transduction processes. No specific diagnostic phenotypes were associated with the subset of suicide deaths with the identified rare variants. These findings suggest an important role for rare variants in suicide risk and implicate genes and gene pathways for targeted replication. - Source: PubMed
Publication date: 2021/05/27
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