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
- Small extracellular vesicles (sEVs) are critical mediators of tumor microenvironment communication, largely through the selective transfer of microRNAs (miRNAs) that reprogram recipient cells. Active miRNA sorting into sEVs depends on RNA‑binding proteins (RBPs), sequence determinants, and RNA modifications. Here, a functional interplay between the RBP SYNCRIP and N6‑methyladenosine (m6A) RNA methylation controlling miRNA loading into hepatocellular carcinoma (HCC)‑derived sEVs has been disclosed. It is reported that (i) METTL3 (Methyltransferase-like-3)‑dependent m6A modification is required for efficient binding of SYNCRIP to specific miRNAs, thereby enabling their selective incorporation into sEVs; (ii) silencing of SYNCRIP markedly reshapes the sEV miRNA-cargo and impairs the ability of HCC‑derived sEVs to induce epithelial-to-mesenchymal transition (EMT) in non‑tumorigenic hepatocytes. Notably, (iii) depletion of METTL3 produces an even stronger effect, indicating that m6A methylation represents an upstream and essential determinant of SYNCRIP‑mediated miRNA export. Mechanistically, the data identify SYNCRIP as an m6A‑dependent miRNA reader, adding epitranscriptomic regulation to sequence‑based miRNA sorting into sEVs. Functionally, disruption of this interaction attenuates sEV‑driven EMT and pro‑tumorigenic signaling. Collectively, these findings uncover a novel regulatory axis governing sEV miRNA cargo selection and highlight the m6A-SYNCRIP interplay as a potential therapeutic target to interfere with sEV‑mediated tumor progression and metastasis. - Source: PubMed
Publication date: 2026/06/15
Quattrocchi LucaGarbo SabrinaMarocco FrancescoRenne Maria MatildeLoria MarcoPucci MarziaCostanzo ElisaBrizzi Maria FeliceFontana SimonaBattistelli CeciliaTripodi Marco - Eggs of many species accumulate thousands of dormant mRNAs that are translated after fertilization at specific times and locations to direct development. However, how embryos coordinate translation of these mRNAs remains unclear. In this study, we identify sequential waves of translation critical for proper development progression. The first wave occurs within 1 h and includes translation of ewsr1b mRNA that harbors a short 3' untranslated region (UTR) comprising 16 nucleotides. The resulting Ewsr1b protein triggers the second translation wave through binding cytoplasmic mRNAs, including pou5f3, which encodes a transcription factor promoting zygotic genome activation. In contrast, HuR and Syncrip repress translation until the first and second waves, respectively. ewsr1b mRNA that has a long 3' UTR is translated in the second wave, and the 3' UTR's length determines protein localization and function. Overall, our findings reveal previously unknown molecular principles that coordinate translation timings and protein functions to drive long-term, multilayered processes. - Source: PubMed
Publication date: 2026/06/13
Sato KeisukeFierro LudivineSuginishi AnyuSanada TakahiroKotani Tomoya - Identifying reliable biomarkers for prion diseases remains a challenge, particularly for early detection in accessible body fluids. A recent mass spectrometry study on the cerebrospinal fluid proteome identified and validated five proteins significantly dysregulated in the preclinical stage of naturally scrapie-affected sheep. In this study, we quantified these proteins in serum and analysed their distribution and gene expression in the central nervous system, correlating these results with characteristic prion-related neuropathological features. Significantly elevated serum levels of synaptotagmin binding, cytoplasmic RNA interacting protein (SYNCRIP), phospholipase D3 (PLD3) and cathepsin D (CTSD) were detected in preclinical animals, mirroring previous cerebrospinal fluid findings. Central nervous system analyses on these three proteins together with osteopontin (SPP1) and complement component 4 (C4) revealed early and region-specific reduced immunoreactivity alongside upregulated gene expression in scrapie-affected animals, correlating significantly with prion-associated neuropathological features. Together, these findings highlight the potential of SYNCRIP, PLD3 and CTSD as promising minimally invasive biomarkers to diagnose prion diseases from the preclinical stage and provide new insights into the spatiotemporal regulation of the five proteins in the central nervous system throughout the progression of disease. Further research is needed to clarify the peripheral biomarker dynamics in relation to the neurodegenerative pathology. - Source: PubMed
Publication date: 2026/06/02
Pérez-Lázaro SoniaBarrio TomásSevilla EloisaBolea RosaBadiola Juan J - Preterm birth (PTB, < 37 weeks of gestation) is a major public health concern in the United States, with Black women experiencing a higher incidence compared to White women. Although some studies have identified social, medical, and obstetric risk factors for PTB, the biological mechanisms underlying spontaneous PTB (sPTB) risk remain unclear. We conducted a secondary analysis using data from Black participants enrolled in the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-be (nuMoM2b), (n = 1073) from 2010 to 2013. Peripheral whole blood samples were collected from all participants between 6 + 0/7 and 13 + 6/7 weeks of gestation. Demographic, behavioral and clinical data were gathered through surveys, and pregnancy outcomes were obtained through chart abstraction. We used the Infinium Methylation EPIC v2.0 BeadChip for epigenome-wide association (EWAS) of DNA methylation and sPTB. - Source: PubMed
Publication date: 2026/05/24
Zhao TingtingZhao YihongReho PaoloSamari GoleenWapner RonaldHazi ArielleWu HaotianBarcelona Veronica - Cell competition, the context-dependent cell elimination phenomenon via short-range cell-cell interactions, was originally described in Drosophila, where heterozygous ribosomal protein (Rp) mutant cells are outcompeted by wild-type neighbors. The transcription factor Xrp1 mediates most Rp phenotypes, including reduced translation and competitiveness, yet how RpS12 induces Xrp1 was unclear. We show that RpS12 promotes a splice variant of Xrp1 encoding the Xrp1 isoform, which defines the Rp loser identity. RpS12 overexpression is sufficient to induce Xrp1 and confer loser status. Expression of either Xrp1 or Xrp1 isoform can trigger competition, establishing Xrp1 as the central driver of the loser fate. When the number of losers exceeds a critical threshold, a quorum-like response supports their survival by post-transcriptionally downregulating Xrp1. We identify the RNA-binding protein Syncrip, reduced in Rp cells, as an Xrp1 regulator whose depletion activates Xrp1-dependent competition. Therefore, RpS12-dependent Xrp1 expression emerges as the primary Rp signal initiating cell competition. - Source: PubMed
Publication date: 2026/05/22
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