CBX2
- Known as:
- CBX2
- Catalog number:
- Y213592
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CBX2
Related genes to: CBX2
- Gene:
- CBX2 NIH gene
- Name:
- chromobox 2
- Previous symbol:
- CDCA6
- Synonyms:
- MGC10561
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-25
- Date modifiied:
- 2015-11-24
Related products to: CBX2
Related articles to: CBX2
- Decidualization is essential for embryo implantation and maintenance of pregnancy, during which quiescent endometrial stromal fibroblasts proliferate and differentiate into decidual stromal cells. Emerging evidence indicates that epigenetic regulators, including histone modifications, play critical roles in uterine receptivity, implantation, and stromal cell decidualization. Our previous study demonstrated that loss of histone deacetylase 3 (HDAC3) impairs endometrial receptivity and decidualization, resulting in female infertility. However, the genome-wide transcriptomic alterations responsible for defective decidualization in loss of HDAC3 remain unclear. In this study, uterine-specific Hdac3 knockout (PgrHdac3; Hdac3) mice exhibited decidual defects following 3 days of artificial decidualization. RNA sequencing analysis of uteri from control and Hdac3 mice revealed widespread dysregulation of genes and pathways associated with decidualization. Pathway analysis identified significant alterations in RHOA, AMPK-NOTCH1-HEY1, and oxidative stress-induced senescence signaling, implicating dysregulation of cytoskeletal remodeling, cellular metabolism, and oxidative stress responses in the HDAC3-mediated decidual response. Notably, expression of Limk1, Prkag1, and Cbx2 for key regulators of these pathways was significantly reduced in Hdac3 mice compared with controls. These findings demonstrate that HDAC3 is a key regulator of the transcriptional and signaling networks required for successful decidualization. Collectively, our study provides a comprehensive transcriptomic profile of HDAC3-deficient uteri and uncovers key molecular mechanisms underlying impaired decidualization, thereby advancing our understanding of uterine function and pregnancy establishment. - Source: PubMed
Nguyen Loan Thi KimTran Dinh NamNahar ShamsunKim Tae HoonJeong Jae-WookYoo Jung-Yoon - Drug resistance jeopardizes the prognosis of high-grade serous ovarian carcinoma (HGSOC) patients via DNA damage repair-coupled mechanism. The role of biomolecular phase separation in DNA damage repair has loomed. Here we find that CBX2 condensates are associated with drug resistance and contribute to DNA double-strand break (DSB) repair in HGSOC. Specifically, CBX2 condensates facilitate the recruitment of key DSB repair factors PARP1, 53BP1, and BRCA1 to chromatin. Patients with a CBX2-negative pattern exhibit the best prognosis, followed by those with non-condensate CBX2, while the worst outcomes are observed in patients with condensate CBX2. By drug screening, Ibrutinib is identified as an effective inhibitor of HGSOC cells and patient-derived organoids with CBX2 condensates. Overall, CBX2 phase separation enhances DSB repair-mediated drug resistance in HGSOC cells, and Ibrutinib may offer a viable therapeutic option for CBX2-positive HGSOC patients. - Source: PubMed
Publication date: 2026/03/26
Sun SiHuang LinMa YujiaWei ZhengZhu MengnaChen MengqingYing FeiquanZhou XiaolingYang PingWen YipingYang QiangCai LiqiongZhang YuanCai Jing - Phase separation is increasingly recognized in facultative heterochromatinization of Polycomb target genes; however, the mechanisms underlying this process remain obscure. Using single-molecule imaging and tracking, we show that individual condensates in mouse embryonic stem cells (mESCs) contain approximately 3 CBX2 molecules and numerous Polycomb repressive complex (PRC)1 and PRC2 subunits and indicate that the composition and dynamics of condensates are developmentally regulated. We reveal that CBX2 clusters PRC2 and controls the spatial distribution of both PRC2 and H3K27me3. Using genomic approaches, we demonstrate that CBX2 binds to condensate initiation sites, which are enriched for PRC2 nucleation sites. CBX2 deletion causes PRC2 and H3K27me3 to redistribute from their regular targets. By developing a separation-of-function variant, we determine that CBX2 relies on its self-clustering ability to function. These findings collectively support a phase-separation model driven by nucleation and bridging, in which low-abundance proteins self-cluster to initiate condensate assembly, a process tightly coupled to function. - Source: PubMed
Publication date: 2026/03/04
Ingersoll StevenTrouth AbbyAngel J CarlosLuo XinlongEspinoza AxelWen JoeyZhu ChengjieTucker JosephAstatike KalkidanPhiel Christopher JSabaawy HatimKutateladze Tatiana GWu Tao PYao TingtingLu ChaoRamachandran SrinivasRen Xiaojun - Lung adenocarcinoma is the most common form of lung cancer with a 5-year survival rate of 15%, largely due to asymptomatic metastasis and late diagnosis. Overexpression of Polycomb group (PcG) proteins, particularly EZH2, the catalytic component of Polycomb Repressive Complex 2 (PRC2), has been associated with the pathogenesis of lung cancer, frequently showing correlation with cancer progression and poor prognosis. In this study, EZH2 levels were modulated by CRISPR/Cas9 gene editing and PRC2 activity was inhibited with EZH2 inhibitor EPZ6438 or EED inhibitor MAK683. gene editing reduced cell proliferation, migration, invasion, and colony formation and reduced NFκ-B signaling activation, indicating an antitumoral effect in vitro. Moreover, EZH2 inhibition also increased the expression of differentiation-related genes, such as , , and lung surfactants, indicating a pro-differentiation effect. However, EZH2-edited cells injected into an immunocompromised mouse model generated larger tumors compared to unedited cells. This was accompanied by increased expression of other PcG genes, including , , , , and , suggesting a compensatory interaction between PRC2 and PRC1 complexes. These findings provide significant clinical relevance, both in elucidating the mechanisms of novel molecular targets and in guiding treatment strategies for lung cancer when using epigenetic inhibitors. - Source: PubMed
Publication date: 2026/01/29
Menezes Joice Mde Mello Diego CSaito Kelly CKimura Edna TFuziwara Cesar S - Among the disorders of sex development (DSD) with karyotype 46,XY, there is a group of diseases caused by defects of androgen synthesis. The last stage of in the synthesis of androgens is the conversion of testosterone into a more active androgen dihydrotestosterone, which occurs under the influence of the enzyme 5α-reductase type II (SRD5A2). SRD5A2 deficiency is a rare disease with autosomal recessive inheritance. - Source: PubMed
Publication date: 2025/12/02
Kalinchenko N YMakretskaya N AKolodkina A AKareva M ATiulpakov A N