KIAA1604 Blocking Peptide
- Known as:
- KIAA1604 Blocking Peptide
- Catalog number:
- 33r-8191
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- KIAA1604 Blocking Peptide
Related genes to: KIAA1604 Blocking Peptide
- Gene:
- CWC22 NIH gene
- Name:
- CWC22 spliceosome associated protein homolog
- Previous symbol:
- -
- Synonyms:
- KIAA1604, EIF4GL, fSAPb, NCM
- Chromosome:
- 2q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-11-27
- Date modifiied:
- 2016-08-08
Related products to: KIAA1604 Blocking Peptide
Related articles to: KIAA1604 Blocking Peptide
- (weeping lovegrass) is a perennial forage grass in which diploid genotypes reproduce sexually whereas polyploids display pseudogamous diplosporous apomixis. Understanding the molecular basis of this reproductive system is important for the potential use of apomixis in crop improvement. Here, we applied a comparative gene expression analysis to identify and functionally assess candidate genes associated with apomictic reproduction in . - Source: PubMed
Publication date: 2026/04/15
Garbus IngridSelva Juan PabloBellido AndrésPasten María CieloCarballo JoséGallo Cristian AMendes Marta ASharbel Timothy FEchenique Viviana C - Splicing factors play a fundamental role in gene expression. Several splicing factors are highly expressed in cancers and promote cell proliferation. Although targeting splicing factors prolongs the duration of G2/M phase, the involvement of splicing factors in the regulation of mitotic checkpoint signaling remains unclear. In this study, we found that knockdown of the splicing factor CWC22 increased not only the population of G2 phase and mitotic cells but also that of tetraploid cells. Notably, CWC22 knockdown induced mitotic slippage, which exhibited premature mitotic exit without spindle assembly checkpoint (SAC) satisfaction following prolonged prometaphase duration. CWC22 knockdown led to cyclin B1 degradation and accumulation of inactive cyclin-dependent kinase 1 with inhibitory phosphorylation at Tyr15 in mitosis. Simultaneous cyclin B1 overexpression and Wee1 blockade mitigated the shortened mitotic duration caused by CWC22 knockdown. RNA-Seq analysis indicated that CWC22 knockdown downregulated SAC-regulatory genes, including BubR1. The shortened mitotic duration caused by CWC22 knockdown was also mitigated by both overexpression of BubR1 and Wee1 blockade. Public datasets showed that CWC22 was highly expressed in pancreatic or cervical cancers, and higher expression negatively correlated with patient prognosis. Targeting CWC22 induced cancer cell death following mitotic slippage and a prolonged G2 phase because of DNA damage accumulation. These results suggest that highly expressed CWC22 contributes to the progression of G2/M phase and prevents mitotic slippage-caused whole-genome doubling by maintaining the SAC function and cyclin-dependent kinase 1 activity in cancer cells. These findings reveal a novel splicing factor function in mitotic checkpoint signaling, which enables uncontrolled cell proliferation in CWC22-overexpressing cancer cells. - Source: PubMed
Publication date: 2026/01/12
Yuki RyuzaburoSaito YouheiNakayama Yuji - The DExD/H-box RNA helicase Prp22 catalyzes messenger RNA (mRNA) release from the spliceosome, and has also been implicated in proofreading the 3' splice site (3'SS), preventing exon ligation of mutant pre-mRNAs through an ATP-dependent mechanism. However, here we reveal an unexpected role for Prp22 in promoting exon ligation of both wild-type and mutant pre-mRNAs by stabilizing Slu7's association with the spliceosome prior to exon ligation. Notably, ATP binding, rather than hydrolysis, by Prp22 inhibits exon ligation of 3'SS mutant pre-mRNA. Following exon ligation, Prp22-mediated ATP hydrolysis facilitates the dissociation of both Slu7 and mRNA from the spliceosome. Remarkably, Prp22 and Cwc22, which bind the 3'- and 5'-exons respectively, remain associated with the released mRNA, whereas Slu7 and Fyv6 dissociate independently. We propose that Prp22 facilitates exon ligation by stabilizing Slu7 binding, with binding of ATP by Prp22 potentially destabilizing that interaction, thereby weakening contacts between the 5'-exon and the 3'SS to inhibit exon ligation. After exon ligation, Prp22-driven ATP hydrolysis induces a conformational change in Prp8 that disrupts its interdomain interactions, enabling mRNA release through the domain interfaces, with Prp22 and Cwc22 remaining associated with the released mRNA. - Source: PubMed
Chung Che-ShengTseng Chi-KangChen Hsin-ChouCheng Soo-Chen - The exon junction complex (EJC) is a key player in metazoan mRNA quality control and is placed upstream of the exon-exon junction after splicing. Its inner core is composed of Magoh, Y14, eIF4AIII and BTZ and the outer core of proteins involved in mRNA splicing (CWC22), export (Yra1), translation (PYM) and nonsense mediated decay (NMD, UPF1/2/3). Trypanosoma brucei encodes only two genes with introns, but all mRNAs are processed by trans-splicing. The presence of three core EJC proteins and a potential BTZ homologue (Rbp25) in trypanosomes has been suggested to adapt of the EJC function to mark trans-spliced mRNAs. We analysed trypanosome EJC components and noticed major differences between eIF4AIII and Magoh/Y14: (i) whilst eIF4AIII is essential, knocking out both Magoh and Y14 elicits only a mild growth phenotype (ii) eIF4AIII localization is mostly nucleolar, while Magoh and Y14 are nucleolar and nucleoplasmic but excluded from the cytoplasm (iii) eIF4AIII associates with nucleolar proteins and the splicing factor CWC22, but not with Y14 or Magoh, while Magoh and Y14 associate with each other, but not with eIF4AIII, CWC22 or nucleolar proteins. Our data argue against the presence of a functional EJC in trypanosomes, but indicate that eIF4AIII adopted non-EJC related, essential functions, while Magoh and Y14 became redundant. Trypanosomes also possess homologues to the NMD proteins UPF1 and UPF2. Depletion of UPF1 causes only a minor reduction in growth and phylogenetic analyses show several independent losses of UPF1 and UPF2, as well as complete loss of UPF3 in the Kinetoplastida group, indicating that UPF1-dependent NMD is not essential. Regardless, we demonstrate that UPF1 depletion restores the mRNA levels of a PTC reporter. Altogether, we show that the almost intron-less trypanosomes are in the process of losing the canonical EJC/NMD pathways: Y14 and Magoh have become redundant and the still-functional UPF1-dependent NMD pathway is not essential. - Source: PubMed
Publication date: 2025/03/07
Gabiatti Bernardo PapiniFreire Eden RibeiroOdenwald Johannade Freitas Nascimento JanainaHoletz FabiolaCarrington MarkKramer SusanneZoltner Martin - Bisphenol A (BPA), a ubiquitous environmental endocrine disruptor, is suspected of disturbing brain development through largely unknown cellular and molecular mechanisms. In the central nervous system, oligodendrocytes are responsible for forming myelin sheaths, which enhance the propagation of action potentials along axons. Disruption of axon myelination can have lifelong consequences, making oligodendrocyte differentiation and myelination critical stages of brain development. In the present study, mice were exposed to BPA during gestation and lactation through drinking water at concentrations of 25 and 250 μg.L. These doses, corresponding to estimated exposures of 4 μg.kg.d and 40 μg.kg.d, respectively, led to disturbances in lipid remodeling associated with myelination in the offspring. Importantly, changes in myelin lipid composition were selectively observed in female mice and were transient, being visible only at post-natal day P15 but not at later stages (P30 and P60). In females exposed to BPA, myelin exhibited a lower proportion of phosphatidylcholines and higher proportions of other glycerophospholipid subclasses, thus resembling more mature myelin. Conversely, male myelin was not affected, likely due to its already more mature lipid composition. Additionally, transcriptomic analysis of female oligodendrocytes at P15 did not reveal any transcriptional changes in genes related to lipid metabolism, further suggesting post-transcriptional effects of BPA via chaperone-mediated protein folding and RNA splicing. In males, the altered genes were mainly associated with synaptic transmission. Finally, alterations in chromatin accessibility were also largely sex dependent and did not correlate with transcription, with the exception of the Cwc22. At this locus, BPA exposure increased chromatin accessibility in half of mice of both sexes, leading to an "unchanged/open" bimodal profile correlated with "unchanged/upregulated" gene expression. Together, these results open new insights into the sex-dependent mechanisms of BPA's effects on brain development. - Source: PubMed
Publication date: 2024/12/30
Naffaa VanessaVan Steenwinckel JulietteMagny RomainRegazzetti AnneKeime CélineGressens PierreLaprévote OlivierAuzeil NicolasSchang Anne-Laure