CDKN1B Antibody
- Known as:
- CDKN1B Antibody
- Catalog number:
- abx000672
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CDKN1B Antibody
Related genes to: CDKN1B 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 Antibody
Related articles to: CDKN1B Antibody
- Approximately 5% of pituitary adenomas (PA) are familial, linked to germline variants in AIP, or syndrome-related genes like MEN1. While somatic GNAS and USP8 variants predominate in specific subtypes, PAM and CABLES1 genes are emerging. - Source: PubMed
Publication date: 2026/04/27
Martinez de Lapiscina IdoiaBaquero CandelaSantos AliciaMolina Ana RosaMoure Maria DoloresAramburu MaiteBancalari RodrigoBoronat MauroBueno GloriaCasano-Sancho PaulaFernandez-Ramos ConcepcionGarcia-Garcia EmilioGonzalez AmparoGonzalez-Rivera NatividadGuerrero-Fernandez JulioHernandez Maria IsabelPaja MiguelPortillo NancyRica ItxasoMoreno Alfonso Soto-Suarez-Ortega LarisaVela AmaiaCastaño LuisValdes Nuria - Hormone receptor-positive (HR + ), HER2-negative breast cancer comprises ~70% of all breast cancer cases and is primarily treated with endocrine therapies such as tamoxifen, aromatase inhibitors, fulvestrant, and CDK4/6 inhibitors. However, resistance arises in ~40% of patients, limiting therapeutic efficacy. - Source: PubMed
Publication date: 2026/04/22
Ahmad SuhailButle AshwinKarn AkshaySunder RomaMishra RohitBawaskar BhargaviParab PallaviRaje VividhChaubal RohanShet TanujaKundu GopalGupta SudeepDutt Amit - Higher levels of manganese (Mn) are encountered in environmental and various occupational settings. Though Mn is an essential trace element required for many biological processes, chronic exposure to higher levels of Mn has been associated with adverse effects on various organs, including the lungs. Recently, we have shown that forced overexpression of microRNA-221-3p (miRNA-221-3p or miR-221-3p) alleviated Mn -induced human pulmonary epithelial cell death. - Source: PubMed
Publication date: 2026/04/12
Punniyasekaran YokeshwaranPal Harsha AkshaylalDasmahapatra SajalMahapatra Santanu KarRajasekaran Subbiah - Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease. Traditional treatments such as corticosteroids and immunosuppressants are limited by variable efficacy and severe adverse effects, highlighting the need for novel therapeutic targets and personalized strategies. We performed a systematic multi-omics Mendelian randomization (MR) analysis applying established proteomic and transcriptomic quantitative trait loci (pQTL/eQTL) resources to genome-wide association studies (GWAS) of four GN subtypes: acute, chronic, IgA nephropathy, and membranous nephropathy. Bayesian colocalization was used to strengthen causal inference, while independent replication and meta-analysis were conducted using the FinnGen cohort. Mouse knockout phenotypes, drug reposition, and computational pharmacology algorithm were applied to evaluate translational potential. Proteomic-wide MR revealed MTR as protective in chronic GN and HCK as a risk factor for membranous nephropathy, whereas CD302 and CDKN1B showed protective effects. Transcriptomic-wide MR identified candidate genes across GN subtypes: RECQL, BRSK2, and MGP in acute GN; AFM, CFHR5, and EPHB2 in chronic GN; IL6R, MBL2, and PRSS3 in IgA nephropathy; and TIMP4, HCK, and PEAR1 in membranous nephropathy. Bayesian colocalization analysis provided strong support for shared causal variants (PPH4 > 0.8) for HCK, CD302, TIMP4, PEAR1, PARP1, and FHIT. Replication and meta-analysis in the FinnGen cohort provided additional consistency across datasets, while downstream translational annotations highlighted IL6R, MBL2, C5, and CD55 as potential hub targets within immune and complement-related pathways. This integrative multi-omics study provides novel insights into the genetic architecture and therapeutic landscape of GN, identifying potential therapeutic targets that may inform precision nephrology and drug repurposing. Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype. - Source: PubMed
Publication date: 2026/04/16
Li GuoqiangJianhan FuGu JiashuWang YinhuaiLiu JiachenYang DongZeng DianjieZhao Pengcheng - The subset of pituitary adenomas with a heritable genetic basis is small but clinically striking. Somatotropinomas are amongst the most frequent pituitary adenoma subtypes encountered in this setting, with germline variants being enriched in familial acromegaly kindreds and people with a childhood or adolescent history of GH hypersecretion manifesting as pituitary gigantism. The genetic causes of familial acromegaly and pituitary gigantism include variants in established pituitary adenoma predisposition genes (AIP especially, but also MEN1, CDKN1B, MAX, and PRKAR1A), X-linked acrogigantism due to Xq26.3 microduplications, and McCune-Albright syndrome due to postzygotic gain-of-function GNAS variants. Potential associations include variants in emerging pituitary adenoma predisposition genes including NF1, PRKACB, PAM, and CHEK2. Given the potential for gene-specific therapeutic implications in these diseases, multimodal genetic testing arranged by experienced pituitary subspecialists and conducted in expert, clinically accredited laboratories is needed to fully evaluate the genetic basis of disease. Key investigations include next-generation sequencing, chromosome microarray, and droplet digital polymerase chain reaction. Exploratory research-based genetic testing may help uncover new genetic causes of familial acromegaly kindreds and pituitary gigantism in people with negative results on standard testing, benefiting those being tested as well as advancing our understanding of the heritable basis of somatotropinomas. - Source: PubMed
Publication date: 2026/04/08
De Sousa Sunita M CDaly Adrian F