PAPD4 Blocking Peptide
- Known as:
- PAPD4 Blocking Peptide
- Catalog number:
- 33r-3535
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PAPD4 Blocking Peptide
Related genes to: PAPD4 Blocking Peptide
- Gene:
- TENT2 NIH gene
- Name:
- terminal nucleotidyltransferase 2
- Previous symbol:
- PAPD4
- Synonyms:
- FLJ38499, GLD2, TUT2
- Chromosome:
- 5q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-07
- Date modifiied:
- 2018-04-20
Related products to: PAPD4 Blocking Peptide
Related articles to: PAPD4 Blocking Peptide
- Physiological amyloidogenesis drives the formation of functional amyloids involved in various biochemical pathways. We recently showed that the RNA tailing and decay machinery controls the maturation of intracellular amyloid-like aggregates. This raises the question of whether enzymes that participate in the maturation of physiological amyloids are involved in pathological amyloidogenesis implicated in human proteopathies. Using and mouse models of pathological amyloids, we show that manipulating the RNA tailing-decay axis alters the toxicity of β-amyloid and α-synuclein involved in Alzheimer's and Parkinson's diseases, respectively. The RNA tailing enzymes TENT4b and TENT2 protect against β-amyloid- and α-synuclein-induced toxicity by facilitating the formation of nontoxic amyloidogenic assemblies. In contrast, the RNA exonuclease Exosc10 potentiates pathological amyloid toxicity. Remarkably, Exosc10 depletion prevents cognitive decline and restores memory in two different mouse models of β-amyloid neurotoxicity. Taken together, these results suggest that pathways of physiological amyloidogenesis participate in pathological amyloid etiology. - Source: PubMed
Publication date: 2026/03/18
Bokros MichaelGrunfeld AlexBalukoff Nathan CBouviere JessicaBeurel EléonoreLee Stephen - Small noncoding RNAs (sncRNAs) are subject to 3'-end trimming and tailing activities that impact maturation versus degradation decisions during biogenesis. To investigate the dynamics of human sncRNA 3'-end processing at a global level, we performed genome-wide 3'-end sequencing of newly transcribed and steady-state sncRNAs. This revealed widespread post-transcriptional adenylation of newly transcribed sncRNAs, which came in two distinct varieties. One is characterized by oligoadenylation, which is transient, promoted by TENT4A/4B polymerases, and most commonly observed on unstable small nucleolar RNAs that are not fully processed at their 3'-ends. The other is characterized by monoadenylation, which is broadly catalyzed by TENT2 and, in contrast to oligoadenylation, stably accumulates at the 3'-end of sncRNAs, including Polymerase-III-transcribed (Pol-III) RNAs and a subset of small nuclear RNAs. Monoadenylation inhibits Pol-III RNA post-transcriptional 3'-uridine trimming and extension and, in the case of 7SL RNAs, prevents their accumulation with nuclear La protein and promotes their biogenesis towards assembly into cytoplasmic signal recognition particles. Thus, the biogenesis of human sncRNAs involves widespread mono- or oligoadenylation with divergent impacts on sncRNA fates. - Source: PubMed
Publication date: 2025/12/05
Ocheltree CodySkrable BlakePimentel AnastasiaNicholson-Shaw TimothyLee Suzanne RLykke-Andersen Jens - Long terminal repeat (LTR) retroelements such as endogenous retroviruses (ERVs) utilize host tRNA as a primer for reverse transcription, and are thus susceptible to silencing by small RNAs derived from the 3'-end of mature tRNAs (3'-tRFs). Rigorous quantification reveals that tRNA level are not directly proportional to 3'-tRFs but specific isoacceptor and isodecoder sequences are highly enriched in a pattern conserved between mouse and human. We found 3'-tRFs are 2'-O methylated by the small RNA methyltransferase HENMT1 protecting them from degradation and promoting ERV silencing. In the absence of HENMT1, 3'-tRFs are subjected to non-templated tailing by the terminal nucleotidyltransferases TUT4 and TENT2 that regulate small RNA turnover. Due to the perfect sequence complementarity of 3'-tRFs to endogenous retroviral sequences, they have thousands of targets in mammalian genomes. We conducted a massively parallel reporter assay using , a highly active murine ERV, to determine target site rules for 3'-tRFs. Our results suggest that HENMT1 not only stabilizes germline integrity but also serves transposon control by 3'-tRFs in the soma. - Source: PubMed
Publication date: 2025/05/12
Steinberg Josh ISertznig HeleneDesmarais John JWilken JennaRubio DaisyPeacey MatthewKinney Justin BSchorn Andrea J - The intestinal epithelium, which is protected by mucosal surfaces composed of mucins and other glycoproteins, functions as a selective barrier that absorbs nutrients while preventing the translocation of harmful substances. To understand the mechanisms between mucosal disruption and tissue inflammation, we orally administrated a mucus-disrupting agent, dextran sodium sulfate, to and screened 63 differentially expressed genes (DEGs). Through a database search using bioinformatics tools (CHEA3 and WebGestalt), we identified ELK1 as a potential key transcription factor for the selected DEGs, and among the 63 DEGs, ELK1-related genes, B3GAT3, FIBP, and TENT2 (, , and in ), were selected as the relevant genes that respond to mucus disruption. We confirmed that enterocyte (EC)-specific knockdown by RNAi significantly reduced gut length and increased intestinal stem cell proliferation in . Additionally, in EC-specific -knockdown flies, it was observed that the mucus-production-related genes, and , were specifically reduced, whereas the inflammatory cytokines and were overexpressed. This study provides evidence that is involved in the regulation of intestinal inflammation in and plays a protective role against mucus disruption. Our findings suggest that may be a potential therapeutic target for the treatment of intestinal inflammatory diseases such as IBD. - Source: PubMed
Publication date: 2025/05/07
Lee Seung HunHwang DooseonLee Jang-WonGoo Tae-WonYun Eun-Young - One of the posttranscriptional mechanisms regulating the stability of RNA molecules involves the addition of nontemplated nucleotides to their 3' ends, a process known as RNA tailing. To systematically investigate the physiological consequences of terminal nucleotidyltransferase TENT2 absence on RNA 3' end modifications in the mouse hippocampus, we developed a new knockout mouse. Electrophysiological measurements revealed increased excitability in KO hippocampal neurons, and behavioral analyses showed decreased anxiety and improved fear extinction in these mice. At the molecular level, we observed changes in miRNAs' monoadenylation in KO mouse hippocampus, but found no effect of the TENT2 loss on the mRNAs' total poly(A) tail length, as measured by direct nanopore RNA sequencing. Moreover, differential expression analysis revealed transcripts related to synaptic transmission to be downregulated in the hippocampus of knockout mice. These changes may explain the observed behavioral and electrophysiological alterations. Our data thus establish a link between TENT2-dependent miRNA tailing and the balance of inhibitory and excitatory neurotransmission. - Source: PubMed
Publication date: 2025/05/16
Wardaszka-Pianka PatrycjaKuzniewska BozenaGumiNska NataliaHojka-Osinska AnnaPuchalska MonikaMilek JacekStawikowska AleksandraKrawczyk PawelPauzin Francois PWojtowicz TomaszRadwanska KasiaBramham Clive RDziembowski AndrzejDziembowska Magdalena