Ask about this productRelated genes to: SYNCRIP Blocking Peptide
- Gene:
- SYNCRIP NIH gene
- Name:
- synaptotagmin binding cytoplasmic RNA interacting protein
- Previous symbol:
- -
- Synonyms:
- NSAP1, GRY-RBP, dJ3J17.2, HNRPQ1, hnRNP-Q, HNRNPQ
- Chromosome:
- 6q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-27
- Date modifiied:
- 2016-10-05
Related products to: SYNCRIP Blocking Peptide
Related articles to: SYNCRIP Blocking Peptide
- Stress granules (SGs) are membraneless ribonucleoprotein condensates that form under stress and dissolve during recovery. While assembly mechanisms are well characterized, the temporal organization of disassembly remains incompletely understood. Here, we performed time-resolved proximity proteomics across SG disassembly (0-50min recovery; n = 3) using G3BP1 as bait, identifying 79 proteins with robust temporal dynamics. Unsupervised clustering resolved five kinetic modules: early-increase, early-decrease/late-increase, transient-drop at ~40min, early-decrease, and zig-zag patterns. The transient-drop module was enriched for RNA-processing factors, consistent with transient changes in RNA-processing factor engagement. SYNCRIP, an hnRNP family protein in the early-decrease/late-increase module, showed characteristic biphasic dynamics during recovery. Functional validation demonstrated that SYNCRIP knockdown specifically impairs late-phase SG clearance-increasing granule size at 50min recovery-without affecting formation. Together, our data provide a modular temporal map of SG disassembly and establish SYNCRIP as a functionally validated factor required for late-phase clearance. - Source: PubMed
Publication date: 2026/04/28
Fujita SuguruMurata MiyuRhee Hyun-WooTate Shin-IchiYasuda Kyota - Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in communication, social interaction, and behavioral regulation. Its etiology arises from a combination of genetic vulnerabilities and environmental influences. Bisphenol A (BPA) is an endocrine-disrupting chemical found in plastic-containing materials, including micro- and nanoplastic pollutants. Recent studies have shown that prenatal BPA exposure can alter behavior and the expression of genes related to autism and neurodevelopment. - Source: PubMed
Publication date: 2026/04/17
Sukjamnong SupornSaeliw ThanitPanjabud PawineeThongkorn SurangratKanlayaprasit SongphonLertpeerapan PattanachatHu Valerie WSarachana Tewarit - Nerve injury-induced gene dysregulation in the dorsal root ganglion (DRG) is considered a key molecular basis for neuropathic pain genesis. Circular RNA is emerging as a critical regulator of gene expression. Here, we reported a novel circular RNA circNrip1 formed by back-splicing from exon 3 to exon 2 of the Nrip1 pre-RNA. Peripheral nerve injury upregulates circNrip1, but not Nrip1 mRNA, in injured DRG neurons, at least in part due to increased binding of the RNA-binding protein FUS to Nrip1 pre-RNA, thereby promoting circNrip1 formation. Blocking this upregulation attenuates nerve injury-induced increases in toll-like receptor 2 (Tlr2) mRNA and TLR2 protein levels in injured DRG, as well as nerve injury-induced nociceptive hypersensitivity. Conversely, mimicking this upregulation elevates DRG Tlr2 mRNA and TLR2 protein expression and produces neuropathic pain-like symptoms in naïve mice. Mechanistically, upregulated circNrip1 enhances its binding to the 3'- untranslated region (UTR) of Tlr2 mRNA and to the RNA-binding protein SYNCRIP, thereby recruiting more SYNCRIP to the Tlr2 mRNA 3'-UTR and stabilizing Tlr2 mRNA in injured DRG neurons. Thus, circNrip1 contributes to neuropathic pain by promoting SYNCRIP-triggered stabilization of TLR2 in DRG neurons and represents a promising therapeutic target for intervention. - Source: PubMed
Publication date: 2026/04/09
Feng XiaozhouXiao JifangHuang CongcongJiang Bao-ChunWang BingLi XuDu ShibinBerkman TolgaWen Chun-HsienCai WeihuaSharma DilipWang KunMa LongfeiHu HuijuanTao Yuan-Xiang - During nervous system development, diverse types of neurons and glia are sequentially generated by self-renewing neural stem cells (NSCs). Temporal changes in gene expression within NSCs are thought to regulate neural diversity; however, the mechanisms regulating the timing of these temporal gene transitions remain poorly understood. type 2 NSCs, like human outer radial glia, divide to self-renew and generate intermediate neural progenitors, amplifying and diversifying the population of neurons innervating the central complex, a brain region crucial for sensorimotor coordination. Type 2 NSCs express over a dozen genes temporally, broadly classified as early- and late-expressed genes. A conserved gene, , mediates early-to-late gene expression by activating ecdysone receptor (EcR) expression. However, the timing of EcR expression and, consequently, the transition from early-to-late gene expression remain unknown. This study investigates whether intrinsic mechanisms of cell cycle progression and cytokinesis are required to induce the NSC early-late transition. By generating mutant clones that arrest the NSC cell cycle or block cytokinesis, we show that both processes are necessary for the early-to-late transition. When NSCs are cell cycle or cytokinesis arrested, the early gene Imp fails to be downregulated and persists in the old NSCs, while the late factors EcR and Syncrip fail to be expressed. Furthermore, we demonstrate that the early factor Seven-up is insufficient to drive the transition, despite its normal expression in cell cycle- or cytokinesis-inhibited NSCs. These results suggest that both cell-intrinsic (cell cycle/cytokinesis) and -extrinsic (hormone) cues are required for the early-late NSC gene expression transition. - Source: PubMed
Publication date: 2026/02/18
Morales Chaya Gonzalo NSyed Mubarak Hussain - HNRNPU is an RNA-binding protein with diverse roles in transcriptional and post-transcriptional regulation. Pathogenic genetic variants of HNRNPU cause a severe neurodevelopmental disorder (NDD), but the underlying molecular mechanisms are unclear. Here, we comprehensively investigate the HNRNPU molecular interactome by integrating protein-protein interaction (PPI) mapping, RNA target identification, and genome-wide DNA methylation profiling in human neuroepithelial stem cells and differentiating neural cells. We identified extensive HNRNPU-centered networks, including an association with the mammalian SWI/SNF chromatin-remodeling complex, and uncovered a previously unrecognized role in translation. We present evidence that HNRNPU associates with messenger RNAs (mRNAs) encoding proteins important for neuronal development, including several linked to NDDs. Silencing HNRNPU reprogrammed methylation dynamics at regulatory regions, particularly at active and bivalent promoters of neurodevelopmental transcription factors. Integrative analysis across PPI, RNA, and methylome datasets identified 19 converging genes at all three molecular levels, including NDD genes within the SWI/SNF complex, SMARCA4 and SMARCC2, and RNA-processing machinery such as SYNCRIP. Together, these data showcase HNRNPU as a central coordinator of RNA metabolism and epigenetic remodeling during neural differentiation, linking RNA-binding, chromatin organization, and DNA methylation to the pathogenesis of HNRNPU-related NDDs. - Source: PubMed
Oksanen MarikaMastropasqua FrancescaMazan-Mamczarz KrystynaMartindale Jennifer LYe XuanArora AbishekBanskota NiradGorospe MyriamTammimies Kristiina