HNRPK Blocking Peptide
- Known as:
- HNRPK Blocking Peptide
- Catalog number:
- 33r-6896
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HNRPK Blocking Peptide
Related genes to: HNRPK Blocking Peptide
- Gene:
- HNRNPK NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein K
- Previous symbol:
- HNRPK
- Synonyms:
- CSBP, TUNP
- Chromosome:
- 9q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-15
- Date modifiied:
- 2016-10-05
Related products to: HNRPK Blocking Peptide
Related articles to: HNRPK Blocking Peptide
- Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a highly conserved, multifunctional DNA/RNA-binding protein that regulates gene expression at both transcriptional and post-transcriptional levels. In skeletal muscle, hnRNPK is essential for development, regeneration, and homeostasis, influencing satellite cell activation, myoblast proliferation and differentiation, and myofiber maturation. Its dysregulation is linked to muscle atrophy, degenerative diseases, and impaired regeneration. This review summarizes current knowledge of hnRNPK's molecular structure, subcellular localization and dynamics, and interactions with nucleic acids and proteins. We highlight its roles in myogenic differentiation, gene expression control, signaling pathway cross-talk, and skeletal muscle development. We also discuss the potential of hnRNPK as a diagnostic biomarker and therapeutic target in muscle disorders, and outline key directions for future research to resolve outstanding questions about its complex regulatory functions. Together, these insights provide a framework for advancing muscle biology and improving the management of muscle-related diseases. - Source: PubMed
Ren KejinZhou KailiAn YijiaCheng XiaofangMeng TiantianLi CencenXu HaixiaZhang PengpengXu Yongjie - Oocyte developmental competence relies on the coordinated progression of nuclear and cytoplasmic maturation, driven by the precise translational regulation of stored maternal mRNAs. Using an integrative transcriptomic and translatomic approach, we characterized the dynamic translational landscape of porcine oocytes during maturation. Through cross-species analysis with human and mouse data, we discovered conserved and species-specific translational programs, highlighting a greater translational resemblance between porcine and human oocytes. Comparative profiling further revealed aberrant maternal mRNA translational activation and degradation during in vitro maturation (IVM) vs. in vivo conditions, including defective translational activation of GPLD1 and HNRNPK, which were pinpointed as mechanisms compromising oocyte quality and embryonic development. To further dissect how translational regulation coordinates oocyte nuclear and cytoplasmic maturation, we employed a dbcAMP-induced cell cycle-synchronized model to identify gene sets with cell cycle-dependent and -independent translational activation. Characterization of these groups identified cytoplasmic polyadenylation element binding protein 1 (CPEB1) as a key orchestrator within the translational regulatory network, where it specifically activates the translation of cell cycle-dependent maternal factors through the cytoplasmic polyadenylation elements (CPEs) within 3'UTRs. Collectively, these findings elucidate key translational mechanisms during porcine oocyte maturation and offer a molecular basis for improving in vitro maturation and reproductive efficiency in livestock. - Source: PubMed
Publication date: 2026/05/08
Wang YuFan ZhengangChu XiaoyuZhou KaiWang TingtingGuan JiaqiHu RuifengLi AiminLi WenjingLiu XinZhang XiaWang XiaoqiuMiao Yi-LiangZhou Jilong - Chinese tongue sole (), an economically important mariculture species in China, exhibits pronounced sexual dimorphism in growth, underscoring the importance of elucidating sex regulatory mechanisms for aquaculture development. Heterogeneous nuclear ribonucleoprotein K () critically regulates mammalian reproductive development, yet its role in fish sex regulation remains elusive. Here, we systematically investigated the underlying function and mechanisms of in through integrated molecular cloning, expression profiling, upstream regulatory analysis, functional assays, and transcriptome sequencing. We found that was highly expressed in the gonad and liver, with female-biased expression during gonadal development. Promoter activity assays revealed that and enhanced transcription, whereas and suppressed it. Additionally, was directly targeted by miR-460a-5p in , revealing multi-level transcriptional and post-transcriptional regulation. Functional analyses showed that regulated in a cell type-dependent and dose-sensitive manner: the expression of was both upregulated in -knockdown ovarian cells and -overexpression testicular cells. Interestingly, was upregulated in -knockdown ovarian cells but suppressed in -overexpression testicular cells, which showed the distinct regulation mechanisms in the different sexual programs. Transcriptomic analyses further revealed that several sex-related genes ( with downregulation, etc.) were significantly regulated, and cell development and cycle pathways were dramatically enriched in functional enrichment analyses. This might indicate that overexpression drives testis (CSTE) toward feminization reprogramming through switching and multi-pathway perturbations. Overall, our findings might reveal that , a female-biased gene regulated by miR-460a-5p and transcription factors, influences sex-related gene expression through switching. This study will offer new insights for into sex determination and also provide a potential target for monosex breeding in aquaculture. - Source: PubMed
Publication date: 2026/04/27
Li KaiminYan HaipengLiu QiLi WenjieGao ChengbinChen Songlin - Brain-derived neurotrophic factor (BDNF) modulates synaptic plasticity via activation of TrkB receptors and plays a key role in epileptogenesis, though its molecular mechanisms remain incompletely understood. Here, we examined how BDNF-TrkB signaling regulates synaptic GluN2A-containing NMDA receptors (NMDARs) and impacts network synchronization in cultured hippocampal neurons. BDNF increased synaptic surface expression of GluN2A-NMDARs in rat hippocampal synaptoneurosomes and cultured neurons in a time- and protein synthesis-dependent manner. Mechanistically, we identified a signaling cascade involving hnRNPK, Pyk2, and protein kinase C (PKC) as critical for this effect. Knockdown of hnRNPK or Pyk2, PKC inhibition, or expression of a phosphorylation-deficient Pyk2 mutant prevented BDNF-induced GluN2A synaptic accumulation. Pyk2 phosphorylation at Y402 was required for both basal and BDNF-induced GluN2A expression. Multielectrode array recordings demonstrated that BDNF and GluN2A-NMDARs contribute to enhanced network activity following stimulation. In vivo, BDNF-TrkB signaling mediated increased synaptic GluN2A expression in the hippocampus of rats subjected to the pilocarpine model of temporal lobe epilepsy, confirming a TrkB-dependent mechanism. These findings reveal a BDNF/TrkB-PKC-Pyk2-hnRNPK pathway that regulates GluN2A synaptic expression and neuronal excitability, offering new insights into the molecular basis of synaptic plasticity and epilepsy. - Source: PubMed
Publication date: 2026/05/05
De Luca PasqualinoMele MirandaNapoli FrancescaMshelia PhilemonCosta Rui ODuarte Carlos B - Colorectal cancer (CRC) represents a prevalent and life-threatening malignancy, posing a significant global health challenge. Transcribed ultraconserved regions (T-UCRs), a specific category of long non-coding RNAs (lncRNAs) encoded within the human genome, have been demonstrated to play significant roles in the pathogenesis of multiple cancer types. However, their pathological role in CRC remains largely unexplored. In this study, we investigate two closely spaced T-UCRs, uc.263 and uc.264, located on chromosome 9, both of which are significantly upregulated in CRC tissues. Our findings further reveal that these two T-UCRs originate from a shared precursor RNA, designated as uc.263/264 in CRC cells. The uc.263/264 has been demonstrated to enhance cellular proliferation, growth, migration, and invasion, while simultaneously regulating the cell cycle and apoptosis. Mechanistically, uc.263/264 interacts with heterogeneous nuclear ribonucleoprotein K (hnRNPK), enhancing its protein stability and resulting in increased hnRNPK expression. Furthermore, uc.263/264 activates the Wnt signaling pathway, a process mediated by hnRNPK. Clinically, both uc.263/264 and hnRNPK are overexpressed in CRC patient samples, exhibiting a positive correlation in their expression levels. This suggests a functional regulatory axis between uc.263/264 and hnRNPK in CRC pathology. Collectively, our findings demonstrate that uc.263/264 can interact with the hnRNPK protein and upregulate its expression, thereby activating the Wnt signaling pathway and promoting the progression of CRC. - Source: PubMed
Publication date: 2026/04/30
Zhang YiXu HanWang XinWei ZichenLi GuiqingHou SicongZhao BenhuoYin MinDing YanbingShe QiangDong HongliangLi YaoyaoPang Lei