Ask about this productRelated genes to: PWWP2A Blocking Peptide
- Gene:
- PWWP2A NIH gene
- Name:
- PWWP domain containing 2A
- Previous symbol:
- -
- Synonyms:
- KIAA1935
- Chromosome:
- 5q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-22
- Date modifiied:
- 2011-03-23
Related products to: PWWP2A Blocking Peptide
Related articles to: PWWP2A Blocking Peptide
- - Source: PubMed
Publication date: 2025/02/28
Ponne SaravanaramanChinnadurai Raj KumarKumar RajenderMohanty Aman KumarBrilhante Raimunda Sâmia NogueiraNhung Trinh Thi TrangBaluchamy Sudhakar - The PWWP domain is a conserved motif unique to eukaryotes, playing a critical role in various cellular processes. Proteins containing the PWWP domain are typically found in chromatin, where they bind to DNA and histones in nucleosomes, facilitating chromatin-associated functions. Among these proteins, PWWP-domain containing proteins 2A and 2B (PWWP2A and PWWP2B), identified during the H2A interactome analysis, are DNA methyltransferase-related proteins, that are structurally disordered, except for their PWWP domain. While their precise functions remain to be fully elucidated, PWWP2A and PWWP2B have been implicated in essential processes such as embryonic development, mitotic regulation, adipose thermogenesis, transcriptional control, and DNA damage response. Their involvement in disease pathology is an emerging area of research, with PWWP2B downregulation linked to recurrent gastric cancer, promoting cell proliferation and migration. Literature reveals that the circular RNA, cPWWP2A sequesters miR-203, miR-223, and miR-27, to modulate TGF-β signalling by inhibiting key regulators like SMAD3 and SP3. Additionally, PWWP2A/B proteins may interact with P4HA3, a regulator of the TGF-β/SMAD signalling pathway that influences tumour invasiveness, though the precise nature of this interaction is not yet fully understood. The PWWP2-miRNA-TGF-β axis, particularly the PWWP2-P4HA3 association, provides valuable insights into therapeutic strategies, especially under adverse conditions where this pathway is differentially regulated. Overall, given their essential roles in fundamental cellular processes and their involvement in disease mechanisms, PWWP2A and PWWP2B proteins could be ideal targets for therapeutic intervention. Thus, these proteins occupy a prominent position in the human proteome and epigenetic landscape. - Source: PubMed
Publication date: 2025/01/12
Ponne SaravanaramanChinnadurai Raj KumarKumar RajenderMohanty Aman KumarNogueira Brilhante Raimunda SâmiaTrang Nhung Trinh ThiBaluchamy Sudhakar - The evolutionarily conserved histone variant H2A.Z plays a crucial role in various DNA-based processes, but the mechanisms underlying its activity are not completely understood. Recently, we identified the zinc finger (ZF) protein ZNF512B as a protein associated with H2A.Z, HMG20A and PWWP2A. Here, we report that high levels of ZNF512B expression lead to nuclear protein and chromatin aggregation foci that form in a manner that is dependent on the ZF domains of ZNF512B. Notably, we demonstrate ZNF512B binding to the nucleosome remodeling and deacetylase (NuRD) complex. We discover a conserved amino acid sequence within ZNF512B that resembles the NuRD-interaction motif (NIM) previously identified in FOG-1 and other transcriptional regulators. By solving the crystal structure of this motif bound to the NuRD component RBBP4 and by applying several biochemical and biophysical assays, we demonstrate that this internal NIM is both necessary and sufficient for robust and high-affinity NuRD binding. Transcriptome analyses and reporter assays identify ZNF512B as a repressor of gene expression that can act in both NuRD-dependent and -independent ways. Our study might have implications for diseases in which ZNF512B expression is deregulated, such as cancer and neurodegenerative diseases, and hints at the existence of more proteins as potential NuRD interactors. - Source: PubMed
Wunderlich Tim MariusDeshpande ChandrikaPaasche Lena WFriedrich TobiasDiegmüller FelixHaddad EliasKreienbaum CarlottaNaseer HaniyaStebel Sophie EDaus NadineLeers JörgLan JieTrinh Van TuanVázquez OlallaButter FalkBartkuhn MarekMackay Joel PHake Sandra B - Alterations in kinase genes such as NTRK1/2/3, RET, and BRAF underlie infantile fibrosarcoma (IFS), the emerging entity 'NTRK-rearranged spindle cell neoplasms' included in the latest WHO classification, and a growing set of tumors with overlapping clinical and pathological features. In this study, we conducted a comprehensive clinicopathological and molecular analysis of 22 cases of IFS and other kinase gene-altered spindle cell neoplasms affecting both pediatric and adult patients. Follow-up periods for 16 patients ranged in length from 10 to 130 months (mean 38 months). Six patients were treated with targeted therapy, achieving a partial or complete response in five cases. Overall, three cases recurred and one metastasized. Eight patients were free of disease, five were alive with disease, and two patients died. All cases showed previously reported morphological patterns. Based on the cellularity and level of atypia, cases were divided into three morphological grade groups. S100 protein and CD34 were at least focally positive in 12/22 and 14/22 cases, respectively. Novel PWWP2A::RET, NUMA1::RET, ITSN1::RAF1, and CAPZA2::MET fusions, which we report herein in mesenchymal tumors for the first time, were detected by RNA sequencing. Additionally, the first uterine case with BRAF and EGFR mutations and CD34 and S100 co-expression is described. DNA sequencing performed in 13 cases uncovered very rare additional genetic aberrations. The CNV profiles showed that high-grade tumors demonstrate a significantly higher percentage of copy number gains and losses across the genome compared with low- and intermediate-grade tumors. Unsupervised clustering of the tumors' methylation profiles revealed that in 8/9 cases, the methylation profiles clustered with the IFS methylation class, irrespective of their clinicopathological or molecular features. © 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2024/02/09
Klubíčková NatálieDermawan Josephine KMosaieby ElahehMartínek PetrVaněček TomášHájková VeronikaPtáková NikolaGrossmann PetrŠteiner PetrŠvajdler MariánKinkor ZdeněkMichalová KvětoslavaSzepe PeterPlank LukášHederová StanislavaKolenová AlexandraSpasov Neofit JurievKosemehmetoglu KemalPažanin LeoŠpůrková ZuzanaBaník MartinBaumruk LuděkMeyer AndersKalmykova AntoninaKoshyk OlenaMichal MichalMichal Michael - As an exemplary model for examining molecular mechanisms responsible for extreme phenotypic variations, plumage color has garnered significant interest. The genus features two species, and , that exhibit striking disparities in plumage color. However, the molecular foundation for this differentiation has remained elusive. Herein, we present two high-quality genomes for and , procured using the Illumina and Nanopore technologies. The assembled genome of was 1.12 Gb in size with a contig N50 of 26.82 Mb, while its counterpart was 1.13 Gb in size with a contig N50 of 21.91 Mb. A comparative analysis unveiled three genes (, , and ) with structural variants in the melanogenic pathway. Notably, we also identified a novel gene, PWWP domain containing 2A (), that is related to plumage color, for the first time. Using targeted gene modification analysis, we demonstrated the potential genetic effect of the variant on pigment gene expression and melanin production. Finally, our findings offer insight into the intricate pattern of pigmentation and the role of polygenes in birds. Furthermore, these two high-quality genome references provide a comprehensive resource and perspective for comparative functional and genetic studies of evolution within the genus. - Source: PubMed
Publication date: 2023/11/29
Chong YuqingTu XiaolongLu YingGao ZhendongHe XiaomingHong JieyunWu JiaoWu DongdongXi DongmeiDeng Weidong