HNRPL Blocking Peptide
- Known as:
- HNRPL Blocking Peptide
- Catalog number:
- 33r-1021
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HNRPL Blocking Peptide
Related genes to: HNRPL Blocking Peptide
- Gene:
- HNRNPL NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein L
- Previous symbol:
- HNRPL
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-22
- Date modifiied:
- 2015-08-25
- Gene:
- HNRNPLL NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein L like
- Previous symbol:
- HNRPLL
- Synonyms:
- -
- Chromosome:
- 2p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-30
- Date modifiied:
- 2016-10-05
Related products to: HNRPL Blocking Peptide
Related articles to: HNRPL Blocking Peptide
- The multifunctional RNA-binding protein hnRNPL is implicated in antibody class switching but its broader function in B cells is unknown. Here, we show that hnRNPL is essential for B cell activation, germinal center formation, and antibody responses. Upon activation, hnRNPL-deficient B cells show proliferation defects and increased apoptosis. Comparative analysis of RNA-seq data from activated B cells and another eight hnRNPL-depleted cell types reveals common effects on MYC and E2F transcriptional programs required for proliferation. Notably, while individual gene expression changes are cell type specific, several alternative splicing events affecting histone modifiers like KDM6A and SIRT1, are conserved across cell types. Moreover, hnRNPL-deficient B cells show global changes in H3K27me3 and H3K9ac. Epigenetic dysregulation after hnRNPL loss could underlie differential gene expression and upregulation of lncRNAs, and explain common and cell type-specific phenotypes, such as dysfunctional mitochondria and ROS overproduction in mouse B cells. Thus, hnRNPL is essential for the resting-to-activated B cell transition by regulating transcriptional programs and metabolism, at least in part through the alternative splicing of several histone modifiers. - Source: PubMed
Publication date: 2024/05/14
Subramani Poorani GaneshFraszczak JenniferHelness AnneEstall Jennifer LMöröy TarikDi Noia Javier M - Circular RNAs (circRNAs) are an intriguing class of widely prevalent endogenous RNAs, the vast majority of which have not been characterized functionally. Here, we identified a novel oncogenic circRNA originating from the back-splicing of Exon2 and Exon3 of a tumor suppressor gene, ARHGAP35 (also known as P190-A), termed as circARHGAP35. have observe that circARHGAP35 and linear ARHGAP35 have antithetical expression and functions. Interestingly, circARHGAP35 contains a 3867 nt long ORF with an mA-modified start codon and encodes a truncated protein comprising four FF domains and lacking the Rho GAP domain. Mechanistically, circARHGAP35 protein promotes cancer cell progression by interacting with TFII-I protein in the nucleus. The RNA binding protein, HNRNPL, facilitates the formation of circARHGAP35. Clinically, circARHGAP35 is associated with poor survival in cancer patients. Our findings characterize an oncogenic circRNA and demonstrate a novel mechanism of oncogene activation in cancer by circRNA through the production of a truncated protein. - Source: PubMed
Publication date: 2021/05/01
Li YanChen BingZhao JingjingLi QinChen SiyuanGuo TiananLi YuchenLai HongyanChen ZhiaoMeng ZhiqiangGuo WeijieHe XianghuoHuang Shenglin - Glucose levels in mammals are tightly controlled through multiple mechanisms to meet systemic energy demands. Downregulation of hepatic glucokinase (GCK) during fasting facilitates the transition of the liver from a glucose-consuming to a gluconeogenic organ. Here, we report the transcriptional regulation of hepatic GCK by a long non-coding RNA (lncRNA) named liver GCK repressor (lncLGR). lncLGR is induced by fasting, and physiological overexpression of lncLGR to mimic fasting levels effectively suppresses GCK expression and reduces hepatic glycogen content in mice. Consistently, lncLGR knockdown enhances GCK expression and glycogen storage in fasted mice. Mechanistically, lncLGR specifically binds to heterogenous nuclear ribonucleoprotein L (hnRNPL), which is further confirmed to be a transcriptional repressor of GCK in vivo. Finally, we demonstrate that lncLGR facilitates the recruitment of hnRNPL to the GCK promoter and suppresses GCK transcription. Our data establish a lncRNA-mediated mechanism that regulates hepatic GCK expression and glycogen deposition in a physiological context. - Source: PubMed
Publication date: 2016/02/18
Ruan XiangboLi PingCangelosi AndrewYang LingCao Haiming