CCNB1 & FZR1 Protein Protein Interaction Antibody Pair
- Known as:
- CCNB1 & FZR1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0213
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CCNB1 & FZR1 Protein Interaction Antibody Pair
Related genes to: CCNB1 & FZR1 Protein Protein Interaction Antibody Pair
- Gene:
- CCNB1 NIH gene
- Name:
- cyclin B1
- Previous symbol:
- CCNB
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-10
- Date modifiied:
- 2016-10-05
- Gene:
- FZR1 NIH gene
- Name:
- fizzy and cell division cycle 20 related 1
- Previous symbol:
- -
- Synonyms:
- HCDH1, CDH1, HCDH, FZR, FZR2, KIAA1242, CDC20C
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-31
- Date modifiied:
- 2017-01-20
Related products to: CCNB1 & FZR1 Protein Protein Interaction Antibody Pair
Related articles to: CCNB1 & FZR1 Protein Protein Interaction Antibody Pair
- Wuding chicken, an indigenous avian breed native to China, is known for its high-quality meat and eggs. However, it has a low egg production rate, poor reproductive traits, and strong broody behavior. Ovarian follicle development is essential for egg production and reproduction, being regulated by the hypothalamus-pituitary-ovary (HPO) axis. Despite its significance, the molecular mechanism of this process in Wuding chicken is still unclear. In this study, the expression profiles of the hypothalamus, pituitary and ovary of Wuding chickens during laying and brooding periods were sequenced and analyzed. A total of 590, 423 and 5371 differentially expressed genes were identified in these three tissues, respectively. We selected genes enriched in reproduction-related signaling pathways to construct a protein-protein interaction network. The network showed that there were 17 genes that were hub genes, including CDK1, CCNB1, CDK2, PLK1, CDC20, AURKB, MAD2L1, BUB1, CCNB3, FZR1, BUB1B, CDC6, CCNA1, MAPK11, MCM3, ESPL1 and CHEK1. After isolating and identifying follicular granulosa cells (GCs), we assessed the function of the hub Aurora Kinase B (AURKB) gene within the network. Overexpression and knockdown experiments confirmed that AURKB promoted the synthesis of steroid hormones, estradiol and progesterone, in GCs by regulating the expression of STAR, CYP19A1, HSD3B1, and PTGS2 genes. In addition, AURKB enhanced GC proliferation while inhibiting GC senescence and apoptosis. These findings indicate that AURKB plays a crucial role in follicular development in Wuding chickens, providing valuable insights into their reproductive biology and laying the foundation for improving their brooding characteristics. - Source: PubMed
Publication date: 2025/08/20
Fan XinyangZhu WeiQiu LihuaHan ChunliuMiao Yongwang - In mammals, oocytes are arrested at G2/prophase for a long time, which is called germinal vesicle (GV) arrest. After puberty, fully-grown oocytes are stimulated by a gonadotropin surge to resume meiosis as indicated by GV breakdown (GVBD). CCNB1 is accumulated to a threshold level to trigger the activation of maturation promoting factor (MPF), inducing the G2/M transition. It is generally recognized that the anaphase-promoting complex/cyclosome (APC/C) and its cofactor CDH1 (also known as FZR1) regulates the accumulation/degradation of CCNB1. Here, by using small interfering RNA (siRNA) and messenger RNA (mRNA) microinjection, immunofluorescence and confocal microscopy, immunoprecipitation, time-lapse live imaging, and immunoblotting analysis, we showed that Septin 4 regulates the G2/M transition by regulating the accumulation of CCNB1 via APC/C . Depletion of Septin 4 caused GV arrest by reducing CCNB1 accumulation. Unexpectedly, the expression level of CDC20 was higher in Septin 4 siRNA-injected oocytes than in control oocytes, but there was no significant change in the expression level of CDH1. Importantly, the reduced GVBD after Septin 4 depletion could be rescued not only by over-expressing CCNB1 but also could be partially rescued by depleting CDC20. Taken together, our results demonstrate that Septin 4 may play a critical role in meiotic G2/M transition by indirect regulation of CCNB1 stabilization in mouse oocytes. - Source: PubMed
Publication date: 2021/06/30
Chen LiOuyang Ying-ChunLi JianQiao Jing-YiGu Lin-JianWang Zhen-BoHou YiSchatten HeideSun Qing-Yuan - Forkhead box M1 (FoxM1) transcriptional factor has a principal role in regulating cell proliferation, self-renewal, and tumorigenesis. However, whether FoxM1 regulates endogenous muscle development and regeneration remains unclear. Here we found that loss of FoxM1 in muscle satellite cells (SCs) resulted in muscle atrophy and defective muscle regeneration. FoxM1 functioned as a direct transcription activator of adenomatous polyposis coli (Apc), preventing hyperactivation of wnt/β-catenin signaling during muscle regeneration. FoxM1 overexpression in SCs promoted myogenesis but impaired muscle regeneration as a result of spontaneous activation and exhaustion of SCs by transcriptional regulation of Cyclin B1 (Ccnb1). The E3 ubiquitin ligase Cdh1 (also termed Fzr1) was required for FoxM1 ubiquitylation and subsequent degradation. Loss of Cdh1 promoted quiescent SCs to enter into the cell cycle and the SC pool was depleted by serial muscle injuries. Haploinsufficiency of FoxM1 ameliorated muscle regeneration of Cdh1 knock-out mice. These data demonstrate that the Cdh1-FoxM1-Apc axis functions as a key regulator of muscle development and regeneration. - Source: PubMed
Publication date: 2020/03/09
Chen ZheLi LeiXu ShuangnianLiu ZhilongZhou ChengfangLi ZhigangLiu YuanyuanWu WeiruHuang YongxiuKuang MeiFan ShijunLi HuiLi XiSong GuanbinWu Wen-ShuChen JiepingHou Yu - Oocyte meiotic maturation failure is one of the major causes for female infertility. Meiotic resumption (the G2/M transition) and progression through metaphase I (MI) are two critical stages of oocyte meiotic maturation. Here, we report that centromere protein T (CENP-T), an internal kinetochore protein, plays a critical role in meiotic resumption of mouse oocytes. Depletion of CENP-T by siRNA injection increased the CDH1 (also known as FZR1) level, resulting in increased activity of the anaphase-promoting complex (APC)-CDH1 complex, and further leading to decreased levels of the cyclin protein CCNB1, attenuated maturation-promoting factor (MPF) activity, and finally severely compromised meiotic resumption. The impaired meiotic resumption caused by CENP-T depletion could be rescued by overexpression of exogenous CCNB1 or knockdown of endogenous CDH1. Overexpression of exogenous CENP-T resulted in decreased CDH1 levels, which accelerated the progression of G2/M transition, and accelerated meiotic cell cycle progression after germinal vesicle breakdown (GVBD). Unexpectedly, spindle organization after GVBD was not affected by the overexpression, but the distribution of chromosomes was affected. Our findings reveal a novel role for CENP-T in regulating meiotic progression by acting through CDH1. - Source: PubMed
Publication date: 2020/02/10
Wang YueLi JianDong FengYue WeiOuyang Ying-ChunWang Zhen-BoHou YiSchatten HeideSun Qing-Yuan - Fizzy-related 1 (FZR1) is an activator of the Anaphase promoting complex/cyclosome (APC/C) and an important regulator of the mitotic cell division cycle. Using a germ-cell-specific conditional knockout model we examined its role in entry into meiosis and early meiotic events in both sexes. Loss of APC/C(FZR1) activity in the male germline led to both a mitotic and a meiotic testicular defect resulting in infertility due to the absence of mature spermatozoa. Spermatogonia in the prepubertal testes of such mice had abnormal proliferation and delayed entry into meiosis. Although early recombination events were initiated, male germ cells failed to progress beyond zygotene and underwent apoptosis. Loss of APC/C(FZR1) activity was associated with raised cyclin B1 levels, suggesting that CDK1 may trigger apoptosis. By contrast, female FZR1Δ mice were subfertile, with premature onset of ovarian failure by 5 months of age. Germ cell loss occurred embryonically in the ovary, around the time of the zygotene-pachytene transition, similar to that observed in males. In addition, the transition of primordial follicles into the growing follicle pool in the neonatal ovary was abnormal, such that the primordial follicles were prematurely depleted. We conclude that APC/C(FZR1) is an essential regulator of spermatogonial proliferation and early meiotic prophase I in both male and female germ cells and is therefore important in establishing the reproductive health of adult male and female mammals. - Source: PubMed
Publication date: 2014/02/19
Holt Janet EPye VictoriaBoon EvanStewart Jessica LGarcía-Higuera IreneMoreno SergioRodríguez RubénJones Keith TMcLaughlin Eileen A