FAM46D Blocking Peptide
- Known as:
- FAM46D Blocking Peptide
- Catalog number:
- 33r-5277
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- FAM46D Blocking Peptide
Related genes to: FAM46D Blocking Peptide
- Gene:
- TENT5D NIH gene
- Name:
- terminal nucleotidyltransferase 5D
- Previous symbol:
- FAM46D
- Synonyms:
- MGC26999, CT1.26, CT112
- Chromosome:
- Xq21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-18
- Date modifiied:
- 2019-03-19
Related products to: FAM46D Blocking Peptide
Related articles to: FAM46D Blocking Peptide
- 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 - Human TENT5 family comprises four members (A-D) associated with different diseases of secretory cells. Homozygous mutations in TENT5A cause a rare form of osteogenesis imperfecta due to impaired collagen deposition by osteoblasts. TENT5C is frequently mutated or deleted in patients with multiple myeloma, the cancer of antibody-secreting plasma cells, and TENT5D alterations result in male infertility. TENT5 members are noncanonical poly(A)polymerases that selectively stabilize mRNAs encoding endoplasmic reticulum-imported proteins, thus promoting the expression of secretory cargoes and proteins involved in folding, glycosylation, and trafficking along the secretory apparatus. This specificity has been proposed to be linked to TENT5 localization at the membrane of the endoplasmic reticulum, thanks to their interaction with transmembrane FNDC3 proteins. Recently, key roles of TENT5 proteins have been described in cancer, bone homeostasis, immunity, stemness, and fertility. This review will comprehensively analyze the identified cellular functions of this novel family of secretory tuners in physiological and pathological conditions, highlighting the proposed molecular mechanisms and the remaining open questions. - Source: PubMed
Lacidogna DanielPennacchio SaraMilan Enrico - Gametogenesis is a process in which dysfunctions lead to infertility, a growing health and social problem worldwide. In both spermatogenesis and oogenesis, post-transcriptional gene expression regulation is crucial. Essentially, all mRNAs possess non-templated poly(A) tails, whose composition and dynamics (elongation, shortening, and modifications) determine the fate of mRNA. Moreover, gametogenesis, especially oogenesis, represents a unique instance of the complexity of poly(A) tails metabolism, with oocyte-specific waves of cytoplasmic polyadenylation. In this context, we provide a comprehensive transcriptomic dataset focusing on mRNA poly(A) tail composition and dynamics in murine testes and ovaries. It consists of RNA samples isolated from wild-type and transgenic mice lacking TENT5 polymerases, which can extend poly(A) tails in the cytoplasm. TENT5 deficiencies have serious consequences. For instance, the defect of TENT5D causes infertility in humans. The data described here are generated mainly using the Oxford Nanopore Direct RNA Sequencing (DRS) method, which provides ground-truth information about mRNA molecules, including poly(A) tail length and nucleotide content. For instance, we show the prevalence of uridilated tails in testicular mRNAs. - Source: PubMed
Publication date: 2025/01/10
Czarnocka-Cieciura AgnieszkaBrouze MichałGumińska NataliaMroczek SewerynGewartowska OlgaKrawczyk Paweł SDziembowski Andrzej - Cytoplasmic polyadenylation plays a vital role in gametogenesis; however, the participating enzymes and substrates in mammals remain unclear. Using knockout and knock-in mouse models, we describe the essential role of four TENT5 poly(A) polymerases in mouse fertility and gametogenesis. TENT5B and TENT5C play crucial yet redundant roles in oogenesis, with the double knockout of both genes leading to oocyte degeneration. Additionally, TENT5B-GFP knock-in females display a gain-of-function infertility effect, with multiple chromosomal aberrations in ovulated oocytes. TENT5C and TENT5D both regulate different stages of spermatogenesis, as shown by the sterility in males following the knockout of either gene. Finally, Tent5a knockout substantially lowers fertility, although the underlying mechanism is not directly related to gametogenesis. Through direct RNA sequencing, we discovered that TENT5s polyadenylate mRNAs encoding endoplasmic reticulum-targeted proteins essential for gametogenesis. Sequence motif analysis and reporter mRNA assays reveal that the presence of an endoplasmic reticulum-leader sequence represents the primary determinant of TENT5-mediated regulation. - Source: PubMed
Publication date: 2024/06/22
Brouze MichałCzarnocka-Cieciura AgnieszkaGewartowska OlgaKusio-Kobiałka MonikaJachacy KamilSzpila MarcinTarkowski BartoszGruchota JakubKrawczyk PawełMroczek SewerynBorsuk EwaDziembowski Andrzej - Teratozoospermia is the main pathogenic factor of male infertility. However, the genetic etiology of teratozoospermia is largely unknown. This study aims to clarify the relationship between novel variations in TENT5D and teratozoospermia in infertile patients. - Source: PubMed
Publication date: 2024/01/16
Zhang Ying-TengShen GanZhuo Liang-ChaiYang XueWang Su-YanRuan Tie-ChaoJiang ChuanWang XiangWang YanYang Yi-HongShen Ying