Ask about this productRelated genes to: PHC2 antibody
- Gene:
- PHC2 NIH gene
- Name:
- polyhomeotic homolog 2
- Previous symbol:
- EDR2
- Synonyms:
- HPH2
- Chromosome:
- 1p35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-12
- Date modifiied:
- 2016-10-05
Related products to: PHC2 antibody
Related articles to: PHC2 antibody
- - Source: PubMed
Publication date: 2026/04/02
Pan XueSun XuejiaoXing YufeiZhang ZengliShi Minhua - Diabetes is a leading cause of mortality globally, with a growing prevalence in low- and middle-income countries. The increasing burden of diabetes has led to a surge in diabetic retinopathy (DR), a major cause of preventable blindness, emphasizing the need to address poor screening practices. - Source: PubMed
Publication date: 2025/10/31
Qureshi AsraFatima MahamJalaluddin ShirinDamji KarimTayyab HaroonKhan Unab I - DNA double-strand breaks (DSBs) are harmful lesions and major sources of genomic instability. Studies have suggested that DSBs induce local transcriptional silencing that consequently promotes genomic stability. Several factors have been proposed to actively participate in this process, including Ataxia-telangiectasia mutated (ATM) and Polycomb repressive complex 1 (PRC1). Here, we found that disrupting PRC1 clustering disrupts DSB-induced gene silencing. Interactome analysis of PHC2, a PRC1 subunit that promotes the PRC1 clustering, found several nucleoporins found in the nuclear pore complex (NPC). Similar to PHC2, depleting the nucleoporins also disrupted the DSB-induced gene silencing. We found that some of these nucleoporins, such as NUP107 and NUP43, which are members of the Y-complex of NPC, localize to DSB sites. The presence of nucleoporins and PHC2 at DSB regions was interdependent, suggesting that they act cooperatively in the DSB-induced gene silencing. We further found two structural components within NUP107 to be necessary for the transcriptional repression at DSBs: ATM/ Ataxia telangiectasia and Rad3-related-mediated phosphorylation at the Serine37 residue within the N-terminal disordered tail and the NUP133-binding surface at the C-terminus. These results provide a functional interplay among nucleoporins, ATM, and the Polycomb proteins in the DSB metabolism and underscore their emerging roles in genome stability maintenance. - Source: PubMed
Publication date: 2025/05/29
Song HongseonBae YubinKim SanginDeascanis DanteLee YujinRona GergelyLane EthanLee Seo-YeoungKim Su-JungPagano MicheleMyung KyungjaeKee Younghoon - The cementation technique using preheated composite resin requires high temperatures for optimal execution and may lead to increased and damaging intrapulpal temperatures. Whether the technique can lead to a temperature increase that might lead to necrosis of the pulp tissue is unclear. - Source: PubMed
Publication date: 2024/09/10
Hatner Hans A OKeigo Rodrigo NCaneschi Camila SAquino Jânio R JAlbuquerque Rodrigo CMorgan Luis Fernando S AMoreira Allyson N - DNA Double-strand breaks (DSBs) are harmful lesions and major sources of genomic instability. Studies have suggested that DSBs induce local transcriptional silencing that consequently promotes genomic stability. Several factors have been proposed to actively participate in this process, including ATM and Polycomb repressive complex 1 (PRC1). Here we found that disrupting PRC1 clustering disrupts DSB-induced gene silencing. Interactome analysis of PHC2, a PRC1 subunit that promotes the formation of the Polycomb body, found several nucleoporins that constitute the Nuclear Pore Complex (NPC). Similar to PHC2, depleting the nucleoporins also disrupted the DSB-induced gene silencing. We found that some of these nucleoporins, such as NUP107 and NUP43, which are members of the Y-complex of NPC, localize to DSB sites. These nucleoporin-enriched DSBs were distant from the nuclear periphery. The presence of nucleoporins and PHC2 at DSB regions were inter-dependent, suggesting that they act cooperatively in the DSB-induced gene silencing. We further found two structural components within NUP107 to be necessary for the transcriptional repression at DSBs: ATM/ATR-mediated phosphorylation at Serine37 residue within the N-terminal disordered tail, and the NUP133-binding surface at the C-terminus. These results provide a new functional interplay among nucleoporins, ATM and the Polycomb proteins in the DSB metabolism, and underscore their emerging roles in genome stability maintenance. - Source: PubMed
Publication date: 2024/07/16
Song HongseonBae YubinKim SanginDeascanis DanteLee YujinRona GergelyLane EthanLee SeoyeongKim SujungPagano MicheleMyung KyungjaeKee Younghoon