Ask about this productRelated genes to: CRNKL1 antibody
- Gene:
- CRNKL1 NIH gene
- Name:
- crooked neck pre-mRNA splicing factor 1
- Previous symbol:
- -
- Synonyms:
- CRN, CLF, SYF3, Clf1
- Chromosome:
- 20p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-05-31
- Date modifiied:
- 2016-10-05
Related products to: CRNKL1 antibody
Related articles to: CRNKL1 antibody
- African swine fever virus (ASFV) causes a highly fatal disease in domestic pigs, resulting in substantial economic losses to the global swine industry. Vaccine development continues to be hindered by limited characterization of viral proteins and their functional redundancies. In this study, we employ combined experimental and computational approaches to characterize the ASFV I73R protein (pI73R), which contains a Z-DNA binding domain and plays a critical role in ASFV virulence and pathogenesis. We demonstrate that pI73R shares significant structural similarity with transcription factors of the forkhead box (FOX) protein family. Overexpression of pI73R results in downregulation of Crooked neck-like protein 1 (CRNKL1), a core spliceosome component, suggesting a potential mechanism by which pI73R modulates host protein synthesis. Using high-resolution mass spectrometry, we map the pI73R interactome and identify the host protein Guanine nucleotide-binding protein subunit beta-1 (GNB1) as a novel direct interactor of pI73R which may facilitate its nuclear transport. Furthermore, we show that pI73R exhibits consistent oligomerization and expression across different ASFV genotypes, highlighting its functional importance. Taken together, these results provide new insights into pI73R function, ASFV-host dynamics, and offer promising directions for antiviral strategy development. - Source: PubMed
Publication date: 2025/12/05
Dolata Katarzyna MagdalenaBettin BarbaraKüchler RichardPannhorst KatrinUshakov Dmitry SFuchs WalterKarger Axel - Tibetan sheep, a critical economic livestock species on the Qinghai-Tibet Plateau, are primarily classified into three types: Plateau Tibetan sheep (PT), Valley Tibetan sheep (VT), and Euler Tibetan sheep (EL). This study was the first to compare the growth performance, meat quality, nutritional composition, transcriptome, and flavor metabolome among these three types of Tibetan sheep. - Source: PubMed
Publication date: 2025/09/29
Li XueHan BuyingLiu DehuiWang SongZhao JincaiWang LeiLi RongBao GuoxiangPei QuanbangSun DeZhang ZianHuang BinZhang FuqiangZhao KaiTian Dehong - Splicing is a complex process that is required to create the transcriptomic diversity needed for specialized functions in higher eukaryotes. The spliceosome contains more than 100 proteins and RNA molecules, which coordinate this dynamic process. Despite the ubiquity of splicing, pathogenic variants in spliceosomal components often cause a tissue-specific phenotype, hinting at further complexities that are not yet fully understood. We have identified a cohort of ten families with de novo missense variants in a spliceosomal component, CRNKL1, where nine individuals harbor one of two missense variants that both affect the same amino acid, Arg267. All affected individuals share a common and specific phenotype: profound pre- and post-natal microcephaly, with pontocerebellar hypoplasia, seizures, and severe intellectual disability. Microinjection of mRNA encoding mutant Crnkl1 into a zebrafish model caused a severe lack of brain development accompanied by a significant reduction in proliferating cells and widespread cellular stress, as indicated by p53 staining. RNA sequencing analysis of injected zebrafish embryos showed broad transcriptomic changes, with altered expression of neuronal and cell cycle genes. Taking these results together, we have identified CRNKL1 as a disease-associated gene and demonstrate the requirement for this protein in brain development. Our findings contribute to a growing disease cluster, where associated components act at the same spliceosomal stage and cause a severe neurological phenotype, suggesting a more intricate role for these spliceosomal subcomplexes than previously thought. - Source: PubMed
Publication date: 2025/06/18
Ray Das SankalitaSullivan RosieRuegg Mischa S GHorsfield JuliaDoran JordanPoke Gemmade Vries NathalieDuerinckx SarahLederer DamienHaniffa MuzhirahKeng Wee-TeikCh'ng Gaik-SiewParry David AJackson Andrew PSakamoto MasamuneMatsumoto NaomichiMiyake NorikoNabatame ShinTaniguchi HidetoshiWakeling Emma Õunap KatrinIlves PilviMirzaa GhaydaTimms AndrewPao EmilyAldinger Kimberly ADobyns WilliamBohring AxelBehre BeateCalame Daniel GLupski James RPascual Juan MAbramowicz MarcGimenez GregoryBicknell Louise S - RNA alternative splicing represents a pivotal regulatory mechanism of eukaryotic gene expression, wherein splicing factors (SFs) serve as key regulators. Aberrant SF expression drives oncogenic splice variant production, thereby promoting tumorigenesis and malignant progression. However, the biological functions and potential targets of SFs remain largely underexplored. Through multi-omics analysis, we identified survival-related splicing factors (SFs) in esophageal cancer and elucidated their biological regulatory networks. To further investigate their downstream splicing targets, we combined alternative splicing events resulting from SF knockdown with those specific to esophageal cancer. Finally, these splicing events were validated through full-length RNA sequencing and confirmed in cancer cells and clinical specimens. We identified six SFs that are highly expressed in esophageal cancer and correlate with poor prognosis. Further analysis revealed that these factors are significantly associated with immune infiltration, cancer stemness, tumor heterogeneity, and drug resistance. was identified as a hub SFs. The target genes and pathways regulated by these SFs showed substantial overlap, suggesting their coordinated roles in promoting cancer stemness and metastasis. Specifically, alternative splicing of key markers, such as CD44 and , was regulated by most of these SFs and correlated with poor prognosis. Our study unveils six survival-related SFs that contribute to the aggressiveness of esophageal cancer and and alternative splicing may act as common downstream effectors of survival-related SFs. This study provides mechanistic insights into SF-mediated tumorigenesis and highlight novel therapeutic vulnerabilities in esophageal cancer. - Source: PubMed
Publication date: 2025/03/27
Gao TianruiFan MeilingZeng ZhongyuanPeng LixiaQian Chao-NanZhao XiaHuang Bijun - Vascular smooth muscle cells(VSMCs) phenotypic switching under hyperglycemic conditions accelerates atherosclerotic progression. Notch receptor 3(NOTCH3), a critical stabilizer of VSMC homeostasis implicated in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) pathogenesis, ensures vascular integrity; however, its interplay with RAN Binding Protein 1() during pathological hyperglycemia remains uncharacterized. We hypothesize that hyperglycemia-induced autophagic dysregulation is mechanistically governed by theNotch receptor 3 ()/ axis, proliferative capacity, and apoptotic signaling in high glucose (HG)-stimulated VSMCs. The aim of this study was to elucidate the regulatory mechanisms of autophagy in VSMCs under HG conditions, with a focus on the / axis and its implications for vascular health. - Source: PubMed
Xu Zhong-JiaoXu JianLei Wen-JingWang XiangZou Qi-LinLv Lin-ChunLiu ChongHu Wu-MingXiang Yi-JiaShen Jia-YiWei Tie-MinZeng Chun-Lai