CDC27 pThr244
- Known as:
- CDC27 pThr244
- Catalog number:
- NB600-464
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CDC27 pThr244
Related genes to: CDC27 pThr244
- Gene:
- CDC27 NIH gene
- Name:
- cell division cycle 27
- Previous symbol:
- D0S1430E, D17S978E
- Synonyms:
- APC3, ANAPC3, NUC2
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-23
- Date modifiied:
- 2017-12-06
Related products to: CDC27 pThr244
ANAPC3,Anaphase-promoting complex subunit 3,APC3,CDC27,CDC27 homolog,CDC27Hs,Cell division cycle protein 27 homolog,D0S1430E,D17S978E,H-NUC,Homo sapiens,Humananti-CDC27 (5C12)anti-CDC27 (C-Terminus)anti-CDC27 (N-Terminus)Anti-CDC27 AntibodyAnti-CDC27 antibodyAnti-CDC27 AntibodyAnti-CDC27 phospho-ser427 AntibodyAnti-CDC27 phospho-ser427 antibodyAnti-CDC27 phospho-thr244 AntibodyAnti-CDC27 phospho-thr244 antibodyAnti-CDC27, Rabbit Polyclonal to CDC27, Isotype , Host Rabbitanti-CDC27, Rabbit polyclonal to CDC27, Isotype IgG, Host RabbitBos taurus,Bovine,CDC27,Cell division cycle protein 27 homologBovine cell division cycle 27 homolog (S. cerevisiae) (CDC27) ELISA kit, Species Bovine, Sample Type serum, plasma Related articles to: CDC27 pThr244
- In animal systems, the only case of third meiotic division without a prior round of DNA replication has been described in Drosophila males carrying mutations in roughex, a gene encoding an inhibitor of Cdk1 activity. Here, we describe another Drosophila gene, terno (teo), that regulates meiotic exit in males. In teo mutants, meiosis I and II are regular, but in many germline cysts, the 64 haploid spermatids undergo an extra division. Additionally, teo mutants are defective in sperm individualization. Teo interacts with cyclin A and B, Fizzy (Cdc20), and the anaphase-promoting complex/cyclosome components Cdc16 and Cdc27. In teo mutant testes, the cyclin A and B levels are higher than in wild type, and downregulation of either cyclin rescues the teo mutant phenotypes. These results suggest that Teo facilitates targeted degradation of the cyclins, so that in teo mutants, there is an increase in Cdk1-CycA and Cdk1-CycB activities, resulting in both the extra meiotic division and the sperm maturation defect. - Source: PubMed
Publication date: 2026/08/13
Bucciarelli ElisabettaGraziadio LuciaPellacani ClaudiaSomma Maria PatriziaMencarelli CaterinaBonaccorsi SilviaGatti Maurizio - Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by uncontrolled proliferation of leukemic cells. Emerging evidence suggests that dysregulation of cell-cycle regulators may interact with immune checkpoint pathways; however, this relationship remains insufficiently explored in AML. To evaluate the expression of CDC27 and PD-L1 in adult AML patients and assess their clinicopathological and prognostic significance. This case - control study included 80 participants: 40 newly diagnosed adult AML patients and 40 age- and sex-matched healthy controls. Gene expression levels of CDC27 and PD-L1 in bone marrow mononuclear cells were quantified using real-time polymerase chain reaction (RT-PCR). Survival analysis was performed and Patients were stratified according to median expression levels. Univariate and multivariate Cox proportional hazards regression analyses were conducted to identify independent prognostic factors. CDC27 and PD-L1 expression levels were significantly higher in AML patients compared with controls ( = 0.001 and = 0.005, respectively). Both markers were associated with adverse clinical features and reduced overall survival. Multivariate analysis identified CDC27 expression as an independent predictor of mortality. Conclusion: CDC27 and PD-L1 overexpression is associated with aggressive disease characteristics and poor survival in AML patients. - Source: PubMed
Publication date: 2026/08/01
Badawy Amira ZakiElkholy Alshimaa Rabie SolimanElkholy Aly MohamedGenena Shaimaa Elsayed RamadanHebesh Eman HelmyEl-Sheity Hanan Hassan - Fetal echocardiography demonstrated a hyperechogenic lesion (possibly calcification) obstructing the tricuspid inflow along with hypoplasia of the right ventricle (RV) and duct-dependent pulmonary circulation. Postnatal inflow along with hypoplasia of the right ventricle (RV) and duct-dependent pulmonary circulation. Postnatal surgical exploration, only minimal antegrade flow was established. Histopathology confirmed degenerative valvar tissue with dense calcification. Eventually, due to persistent inflow restriction and inadequate RV growth, the infant underwent single-ventricle palliation (bidirectional Glenn shunt) with uneventful follow-up after the procedure. This case highlights the extreme rarity of congenital valvular calcification, its possible developmental and genetic associations, and the hemodynamic significance of inflow obstruction in causing ventricular hypoplasia. - Source: PubMed
Publication date: 2026/05/25
Pandey Amit KumarBhat PrernaKottyail BrijeshNair InduKumar Raman KrishnaVaidyanathan Balu - Breast cancer is the most frequently diagnosed cancer worldwide, with approximately 15% classified as Triple-Negative Breast Cancer (TNBC). TNBC is characterized by the absence of estrogen receptor (ER) and progesterone receptor (PR), and the lack of HER2 overexpression, limiting use of targeted therapies. Current TNBC treatment relies heavily on chemotherapy, most commonly taxanes including paclitaxel that stabilize microtubules, disrupt chromosome separation and induce apoptosis. TNBCs frequently develop chemoresistance after multiple treatment cycles, highlighting a critical unmet need for novel therapeutic strategies. This study addresses this challenge by targeting salt-inducible kinase 2 (SIK2), which is overexpressed in 85% of TNBCs compared to normal breast tissue. - Source: PubMed
Publication date: 2026/06/04
Pina Marc AOzyurt RumeysaMao WeiqunYang HailingSantiago-O'Farrill Janice MLu ZhenBast Robert C - Metabolic determinants of oocyte quality and embryonic development remain incompletely understood. Here, we profiled metabolites in human cumulus cells (CCs) and follicular fluid (FF), validated in two mouse models, and integrated transcriptomics with receptor blockade to define mechanisms. In human CCs, adenosine was higher in cycles yielding fewer high-quality embryos and discriminated embryo quality (ROC AUC = 0.75). Conversely, FF adenosine was reduced in the same context. In mice, low-quality oocytes and their associated CCs accumulated adenosine, revealing an intra- vs extracellular disequilibrium. The imbalance aligned with reduced expression of the adenosine transporters ENT1/ENT2 and the gap-junction component CX37. Functionally, supplementation with exogenous adenosine restored early embryonic development from low-quality oocytes, lowering oxidative stress and spindle/chromosome errors via adenosine receptors. Smart-seq2 transcriptomic analysis and functional experiments showed partial normalization of programs governing meiosis and cellular stress responses, including correction of CycB1/Cdc27 (MPF/APC/C) and JNK-linked pathways. Together, we identify adenosine disequilibrium as a metabolic fingerprint of poor oocyte competence and show that receptor-mediated adenosine signaling tunes MPF-related and oxidative stress pathways to rescue developmental potential. These findings provide a mechanistic and translational basis for early prediction and culture optimization in ART. - Source: PubMed
Publication date: 2026/06/09
Yang JihongWang HuiLi YangbaiZhang XinyueFeng TingLi SuyingChen YaoXu YuntianFeng RuizhiChen MinjianQian Yun