FAM46C Blocking Peptide
- Known as:
- FAM46C Blocking Peptide
- Catalog number:
- 33r-5037
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- FAM46C Blocking Peptide
Related genes to: FAM46C Blocking Peptide
- Gene:
- TENT5C NIH gene
- Name:
- terminal nucleotidyltransferase 5C
- Previous symbol:
- FAM46C
- Synonyms:
- FLJ20202
- Chromosome:
- 1p12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-18
- Date modifiied:
- 2019-03-19
Related products to: FAM46C Blocking Peptide
Related articles to: FAM46C Blocking Peptide
- Spatial regulation of mRNA polyadenylation emerges as a key mechanism shaping cellular function. The TENT5/FAM46 family comprises four non-canonical poly(A) polymerases that stabilize transcripts encoding ER-targeted proteins, with mutations linked to diseases of professional secretory cells. Using transcriptomic and proteomic profiling with systematic mutagenesis, we show how paralog-specific divergence drives distinct localization, interactions, and functions. TENT5D, the most ER-associated member, remodels the proteome, enhancing the expression of ER, ERGIC, Golgi, and lysosomal proteins. In contrast, TENT5B lacks ER targeting and regulates proteins involved in cell division. A member-specific C-terminal region that binds ER-transmembrane FNDC3 proteins is necessary and sufficient for ER localization. Mutations in this region of TENT5C, found in multiple myeloma, impair FNDC3 binding or stability, reducing immunoglobulin production and tumor-suppressive activity. Overall, we define a domain-encoded mechanism linking TENT5 localization to transcript selectivity and secretory output, with direct implications for compartmentalized mRNA regulation and development of RNA-based therapeutic strategies. - Source: PubMed
Publication date: 2026/06/04
Viviani LisaLacidogna DanielPennacchio SaraMengozzi Maria VittoriaOrfanelli UgoGiordano LeonePerini TommasoCenci SimoneMilan Enrico - Numerous studies have identified a large number of miRNA editing sites via deep sRNA sequencing profiling of tissue samples. However, the single-cell landscape of miRNA editing patterns has remained largely unknown to date. To investigate miRNA editing and mutation characteristics at single cell level, this study analyzed miRNA editing and mutation events in 448 single-cell small RNA sequencing profiles from 5 different cell types. Our results revealed that PCA and clustering analysis, performed based on the editing levels of identified miRNA editing sites, could distinguish distinct cell types, indicating that miRNA editing patterns are cell-type-specific across different cellular populations. We further demonstrated that a subset of miRNA editing sites exhibited strict cell-type-specific editing patterns. Meanwhile, within the same cell type, the identified sites presented different distributions of editing levels in different cells. A fraction of sites showed highly variable editing levels among different cells of the same cell type, while some sites displayed relatively uniform and consistent editing patterns. An A-to-I editing site in hsa-mir-376c, i.e., hsa-mir-376c 48 A g, showed a significantly higher editing level in glioblastoma cells than in naive embryonic stem cells, suggesting a potential role in the initiation and progression of glioblastoma. Furthermore, our results also suggest that in leukemia cells, TENT4A, TENT5A, TENT5B, TENT5C, TENT5D, and TUT1 may mediate the non-templated nucleotide additions to the 3'ends of miRNAs. - Source: PubMed
Publication date: 2026/04/09
Mao ChunyiGuo HaoXie WenpingXu YueZhang HongjiaLuo KangYang JunZheng Yun - Changes in the poly(A) tail length of Odf1 and other transcripts critical for male fertility have been linked to translational activation during sperm formation. The mRNA poly(A) polymerase TENT5C is required for fastening the flagellum to the sperm head, but its role in shaping the poly(A) tail profile of the spermatid transcriptome remains unclear . Here, we comprehensively document how changes in mRNA poly(A) tail length across the transcriptome reflect transcript metabolism in spermatids. In the absence of TENT5C polymerase activity, Odf1 transcripts show shorter poly(A) tails and, together with ODF1 protein, fail to accumulate at the spermatid neck. Mice expressing a catalytically inactive TENT5C produce headless spermatozoa with flagellar abnormalities associated with ODF1 deficiency . We propose that TENT5C poly(A) polymerase activity regulates the stability and local translation of Odf1 mRNAs at the neck of late-stage spermatids, a process critical for sperm morphogenesis and fertility. These findings highlight the power of poly(A) tail profiling to identify abnormal mRNA processing causative of infertility. - Source: PubMed
Publication date: 2026/04/20
Baptissart MarineGupta AnkitPerez Maira LPoirot Alexander CPapas Brian NGuardia Carlos MMorgan Marcos - FAM46C is a tumor suppressor initially identified in multiple myeloma (MM) but increasingly recognized for its role also in other cancers. Despite its significance, studies exploring the therapeutic potential of FAM46C in combination with targeted treatments remain limited. Sphingosine kinases (SphK1 and SphK2) are key regulators of sphingolipid signaling, a pathway essential for maintaining cell structure and function but frequently deregulated in tumors, making them promising targets for cancer therapy. Preliminary work from our laboratory showed that FAM46C expression synergizes with administration of SKI-I, a pan-inhibitor of sphingosine kinases. In this study, we focused specifically on SphK1, the sphingosine kinase predominantly implicated in cancer and investigated the combinatorial effect of forced FAM46C expression and treatment with PF-543, a selective SphK1 inhibitor. We found that FAM46C overexpression enhances, whereas its downregulation reduces, the cytotoxic efficacy of PF-543 in MM cell lines. Using an in vivo xenograft model, we further validated these findings, showing that FAM46C-expressing MM tumors are indeed sensitive to PF-543 while tumors harboring the D90G loss-of-function variant of FAM46C are not. Overall, our results uncover a novel synergistic interaction between FAM46C expression and SphK1 inhibition, highlighting a promising therapeutic strategy for MM treatment. - Source: PubMed
Publication date: 2025/04/26
Miluzio AnnaritaDe Grossi FedericaMancino MarilenaBiffo StefanoManfrini Nicola - Terminal nucleotidyltransferase 5C (TENT5C) is a noncanonical poly(A) polymerase that promotes cancer suppression. TENT5C has been proposed to mediate the susceptibility of multiple myeloma to treatment with dexamethasone, a steroid hormone analog that binds to the glucocorticoid receptor (GR). However, the relationship between TENT5C and nuclear receptor (NR) signaling remains unclear. In this study, we investigate the regulatory role of TENT5C in the GR and estrogen receptor α (ERα) ligand complexes. We find that TENT5C acts as a corepressor of both GR and ERα. Molecular dynamics simulations indicate that the third TENT5C LXXLL motif directly interacts with ERα, but not GR. The physical interaction of TENT5C and ERα is supported by co-immunoprecipitation assays. Reporter assays show that mutations to the third TENT5C LXXLL motif disrupt TENT5C-mediated repression of ERα but do not affect the repression of the GR complex. In addition, the disruption of TENT5C poly(A) polymerase activity does not appear to affect TENT5C repression of ERα in the cell lines studied. Taken together, our findings highlight a role of TENT5C as an NR corepressor, differentially modulating GR- and ERα-induced transcriptional activity. - Source: PubMed
Publication date: 2025/05/27
Li YinPerera LalithHe Rebecca SBaptissart MarinePetrovich Robert MMorgan Marcos