CDKN1B Mouse Monoclonal Antibody
- Known as:
- CDKN1B Mouse Monoclonal Antibody
- Catalog number:
- BIN-001027-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CDKN1B Mouse Monoclonal Antibody
Related genes to: CDKN1B Mouse Monoclonal Antibody
- Gene:
- CDKN1B NIH gene
- Name:
- cyclin dependent kinase inhibitor 1B
- Previous symbol:
- -
- Synonyms:
- KIP1, P27KIP1
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-14
- Date modifiied:
- 2016-10-05
Related products to: CDKN1B Mouse Monoclonal Antibody
Related articles to: CDKN1B Mouse Monoclonal Antibody
- Multiple endocrine neoplasia (MEN) comprises a group of rare autosomal dominant genetic disorders characterized by the development of benign or malignant tumors in 2 or more endocrine glands, most commonly including the thyroid, parathyroid, pituitary, adrenal glands, and pancreatic neuroendocrine tissues. MEN4 is a recently recognized subtype that phenotypically overlaps with MEN1 and is caused by germline mutations in the cyclin-dependent kinase inhibitor 1B (CDKN1B) gene. However, due to the limited number of reported cases and the lack of standardized clinical guidelines, the clinical characteristics of MEN4 remain insufficiently understood. - Source: PubMed
Publication date: 2026/01/20
Yuke LiuHongxing WangHuiwen TanJianwei LiYerong Yu - Aberrant cell cycle progression is a hallmark of non-small cell lung cancer (NSCLC) and remains a major driver of uncontrolled tumor growth. β-Transducin repeat-containing protein 2 (β-TrCP2), a substrate-recognition component of an E3 ubiquitin ligase complex, has been implicated in diverse cellular processes; however, its role in NSCLC progression is not fully understood. This study aimed to investigate the functional significance of β-TrCP2 in NSCLC cell proliferation and cell cycle regulation. - Source: PubMed
Kim NayunKim JinjuNguyen Hai-AnhMun Se HwanHan SoraYang Young - Premature ovarian insufficiency (POI) impairs fertility and health in reproductive-age women, with autoimmune factors contributing to 4-30% of cases. To investigate immune dysregulation in POI, we developed two mouse models using pZP3 induction: regular immune (RE-POI) and enhanced immune (EN-POI) cycles. The EN-POI model exhibited stable, irreversible ovarian dysfunction, including disrupted estrous cycles, hormonal changes (elevated FSH, decreased AMH, and estradiol), follicular depletion, and infertility. Immune profiling demonstrated consistent T-lymphocyte imbalance across both RE-POI and EN-POI model groups, characterized by expanded splenic CD4 T cells, diminished regulatory T cells, elevated systemic inflammatory cytokines, and ovarian fibrosis. Proteomic comparison between the control and EN-POI groups identified 198 differentially expressed proteins, mainly enriched in immune and inflammatory pathways. Based on these differential proteins, subsequent network analysis further identified six key hub proteins, namely Mmp9, Isg15, Ikbke, Siglec1, Pf4, and Cdkn1b. This study establishes a stable autoimmune POI model, elucidates T-cell imbalance with cytokine storm and fibrosis, and identifies key molecules linking immune abnormalities to ovarian failure, offering new insights into POI research. - Source: PubMed
Publication date: 2026/05/11
Tian YingZhou JiaqiPei XinyiLiu FeiranDiao Feiyang - Cancers reflect aberrant growth and differentiation of normal cell populations. Biological understanding of small intestine neuroendocrine tumors (SI-NETs) is hampered because their closest normal counterparts, enteroendocrine cells (EECs), constitute tiny fractions of intestinal epithelium. Recent characterization of adult human EEC ontogeny from intestinal stem cells can help overcome that limitation. Transient expression of transcription factor gene ASCL1 normally ensures proper timing and fidelity of well-differentiated EECs, which express NEUROD1. Here we report that SI-NETs resembled mature enterochromaffin cells; however, individual tumor cells co-expressed stem/progenitor genes, harboring each differentiation state along the EEC trajectory except ASCL1+ precursors. We found that enhancers normally active, and others inactive, during EEC differentiation underlie aberrant SI-NET gene activity. SI-NETs uniformly expressed NEUROD1 but lacked ASCL1, owing to inaccessible chromatin and repressive H3K27me3 marking at the ASCL1 locus. Multiple cyclin-dependent kinase inhibitor (CDKi) genes were similarly silenced, other than CDKN1B, the only gene recurrently mutated in SI-NETs. Deletion of CDKN1B altered cell cycle kinetics during human EEC differentiation, and deletions of ASCL1 or CDKN1B activated certain genes that are expressed in SI-NETs but not in the normal EEC trajectory. We propose that a limited CDKi repertoire and absence of ASCL1-dependent constraints on EEC maturation together explain unique SI-NET characteristics. - Source: PubMed
Publication date: 2026/05/21
Singh Pratik NpHadj Bachir ElsaHowe James RBellizzi Andrew MCejas PalomaMadha-Krause ShariqEpstein Charles BChan JenniferBernstein Bradley EKulke Matthew HZhou QiaoShivdasani Ramesh A - Pituitary adenomas are increasingly recognised to have a germline genetic component in a subset of patients, particularly those with young-onset disease, familial clustering or syndromic features. The spectrum of germline variants implicated in pituitary tumorigenesis has broadened considerably, with evidence of both established predisposition genes and a growing number of emerging candidate genes. Established germline predisposition genes - namely, MEN1, PRKAR1A, AIP, CDKN1B, GPR101, SDHx and MAX - remain central to our understanding of familial pituitary adenoma predisposition and have defined roles in specific clinical contexts which influence adenoma phenotype, age at presentation, surveillance strategies and family screening. Beyond this, a set of less prevalent variants in other genes - for example, CABLES1, CDH23, PAM, CHEK2 and the mismatch repair (MMR) genes - are emerging as potential contributors, although the pathogenicity and clinical relevance of these genes remain to be fully established. Identifying causative germline variants in people with pituitary adenomas offers the opportunity of personalised care via gene-specific surveillance strategies, prognostication, cascade testing and reproductive planning to the potential benefit of the individual as well as their families. In this review, we provide a clinically-orientated overview of the established and emerging genes implicated in the germline predisposition to pituitary adenomas. We also present a contemporary clinical approach to germline genetic testing in patients with pituitary adenomas. - Source: PubMed
Publication date: 2026/05/16
Mignone EdwardSorvina AlexandraTorpy David JScott Hamish SDe Sousa Sunita M C