CSTF2T 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- CSTF2T 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00023283-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CSTF2T 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: CSTF2T 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- CSTF2T NIH gene
- Name:
- cleavage stimulation factor subunit 2 tau variant
- Previous symbol:
- -
- Synonyms:
- DKFZp434C1013, KIAA0689, CstF-64T, tauCstF-64
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-09
- Date modifiied:
- 2016-10-05
Related products to: CSTF2T 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: CSTF2T 293T Cell Transient Overexpression Lysate(Denatured)
- Alternative RNA processing generates extensive transcript diversity, yet how transcript architecture influences selective m A deposition is incompletely understood. Exon-junction-based models explain where m A is excluded, but a positive determinant of m A accumulation remains undefined. Here, we leverage Zika virus-induced changes in m A deposition to uncover determinants of transcript-selective methylation. By integrating GLORI-seq, native METTL3 RNA immunoprecipitation, and nanopore direct RNA sequencing, we generate a single-nucleotide, isoform-resolved map of m A dynamics during infection. We identify over 2,000 dynamic m A sites, many arising from changes in transcript architecture, and pinpoint proximal polyadenylation sites as positive determinants of m A accumulation. The cleavage stimulation factors CSTF2 and CSTF2T drive this remodeling through two routes: redundant induction of intronic polyadenylation, which converts internal exons into terminal exons that expose DRACH motifs to METTL3, and non-redundant, cleavage-independent recruitment of METTL3 near proximal polyadenylation sites, establishing alternative polyadenylation as a key architectural determinant of the m A landscape. - Source: PubMed
Publication date: 2026/06/08
Aufgebauer Caroline JNelson Theodore MHouerbi NadiaVeenbaas Seth DTegowski MatthewLuo EstherSivasudhan EnakshiGoneos MichaelCollier PaulProszynski JacquelineRyon KristaViolette Evan MTouré Savanna AMeyer Kate DMason Christopher EHorner Stacy M - Approximately one-third of breast cancer (BC) patients show poorer cognitive function (CF). Using DNA methylation (DNAm) data, here we aimed to identify genes and biological pathways associated with CF in postmenopausal women with early-stage hormone receptor-positive (HR+) BC. - Source: PubMed
Publication date: 2025/08/06
Liu ShuweiLiu DongjingBender Catherine MErickson Kirk ISereika Susan MShaffer John RWeeks Daniel EConley Yvette P - Respiratory syncytial virus (RSV) is a major cause of severe respiratory infections, yet effective treatments are lacking. We found that the molecular chaperon DNAJB6/MRJ plays an essential role in RSV replication. Depletion of the long isoform of MRJ (MRJ-L) suppresses RSV replication. Transcriptomic analysis revealed that MRJ-L depletion downregulates Wnt signaling pathways. A pharmacological inhibitor of Wnt signaling suppressed RSV propagation and unexpectedly reduced MRJ-L expression, suggesting a positive regulatory loop between Wnt signaling and MRJ-L expression. Notably, simultaneous inhibition of Wnt signaling and MRJ-L additively suppressed RSV replication, suggesting that the Wnt-MRJ-L axis may serve as a new therapeutic target. This study provides insights into host-RSV interactions and potential antiviral strategies. - Source: PubMed
Publication date: 2025/07/25
Lu Chun-YiLai Peng-YehHuang Jen-MinChang Luan-YinYen Ting-YuTarn Woan-YuhHuang Li-Min - Approximately one-third of breast cancer (BC) patients show poorer cognitive function (CF) before receiving adjuvant therapy compared with age-matched healthy controls. However, the biological mechanisms driving CF variation in the context of BC remain unclear. In this study, we aimed to identify genes and biological pathways associated with CF in postmenopausal women with early-stage hormone receptor-positive (HR+) BC using DNA methylation (DNAm) data, a dynamic regulator of gene activity. - Source: PubMed
Publication date: 2024/11/18
Liu ShuweiLiu DongjingBender Catherine MErickson Kirk ISereika Susan MShaffer John RWeeks Daniel EConley Yvette P - The RNA recognition motif (RRM) is a conserved and ubiquitous RNA-binding domain that plays essential roles in mRNA splicing, polyadenylation, transport, and stability. RRM domains exhibit remarkable diversity in binding partners, interacting with various sequences of single- and double-stranded RNA, despite their small size and compact fold. During pre-mRNA cleavage and polyadenylation, the RRM domain from CSTF2 recognizes U- or G/U-rich RNA sequences downstream from the cleavage and polyadenylation site to regulate the process. Given the importance of alternative cleavage and polyadenylation in increasing the diversity of mRNAs, the exact mechanism of binding of RNA to the RRM of CSTF2 remains unclear, particularly in the absence of a structure of this RRM bound to a native RNA substrate. Here, we performed a series of NMR titration and spin relaxation experiments, which were complemented by paramagnetic relaxation enhancement measurements and rigid-body docking, to characterize the interactions of the CSTF2 RRM with a U-rich ligand. Our results reveal a multistep binding process involving differences in ps-ns time scale dynamics and potential structural changes, particularly in the C-terminalα-helix. These results provide insights into how the CSTF2 RRM domain binds to U-rich RNA ligands and offer a greater understanding for the molecular basis of the regulation of pre-mRNA cleavage and polyadenylation. - Source: PubMed
Publication date: 2024/09/21
Masoumzadeh ElaheLatham Michael P