CDK6 (phospho_Tyr24) Antibody
- Known as:
- CDK6 (phospho_Tyr24) Antibody
- Catalog number:
- E011543-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- CDK6 (phospho_Tyr24) Antibody
Related genes to: CDK6 (phospho_Tyr24) Antibody
- Gene:
- CDK6 NIH gene
- Name:
- cyclin dependent kinase 6
- Previous symbol:
- -
- Synonyms:
- PLSTIRE
- Chromosome:
- 7q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-14
- Date modifiied:
- 2019-04-23
Related products to: CDK6 (phospho_Tyr24) Antibody
Related articles to: CDK6 (phospho_Tyr24) Antibody
- Breast cancer is the most common cancer in women in the UK. For women who have early-stage oestrogen-receptor positive (ER+ve) disease, daily oral adjuvant endocrine therapy reduces risk of recurrence. Recently, CDK4/6 inhibitors, a form of biological therapy, have been approved for use alongside endocrine therapy. However, trial data suggest there may be challenges with adherence to CDK4/6 inhibitors. This study aims to explore the experiences of adherence and support needs of women who have been prescribed CDK4/6 inhibitors for early ER+ve breast cancer. It will also co-develop an intervention to support women with adherence to these drugs alongside endocrine therapy through an evidence-based, theory-informed and patient-centred approach. - Source: PubMed
Publication date: 2026/08/11
Teow PearlinMcGeagh LucyCain HenryTodd AdamRehman FarahBrett JoLevitt NickyTurner MarkStewart Sarah-Jane FHunt EmmaTerrado HazelineWatson EilaSharp Linda - Indigenous chickens in Eritrea are raised mainly in low-input village systems and show marked variation in body size, including reduced body size phenotype, a trait associated with reduced feed consumption, thermotolerance, disease resistance, and adaptability to resource-limited environments. This study aimed to identify genomic regions associated with reduced body size using a genome-wide association study (GWAS) in Eritrean chicken ecotypes. Blood samples from 384 ICs across 16 ecotypes (21 to 24 birds per ecotype) were genotyped using DArTseq technology. Three putative short-bodied ecotypes, Barentu (BAR), Foro (FORO), and Gogne (GOG), were compared with five heavier control ecotypes: Fshe-Mrara (FM), Adi-Tekeliezan (ADTEK), Emni-Haili (HAYL), Dekemhare (DEKE), and Adikeyh (KEIH). After filtering for individual missingness, marker call rate, and minor allele frequency, 141 birds and 42,356 SNP remained. Population structure was evaluated by principal component analysis and ADMIXTURE. Exploratory case-control GWAS were conducted for each putative reduced-body-size ecotype and for the 3 ecotypes combined. Complementary quantitative-trait GWAS used body weight, body length, back length, and shank length was carried out. Linear mixed models implemented in GEMMA included sex as a fixed effect and genomic kinship as a random effect. The first 2 principal components showed extensive ancestry sharing, although GOG was more differentiated. Ecotype-specific analyses identified significant regions near CDK6, BDNF, FOXP1, TNS3, and LGR4 in FORO; EIF2AK2, NANP, MDH1, UGP2 and FGF13 in GOG; and HMGA2, IGF2, BRSK1 and SUCNR1 in BAR. The combined analysis showed no genome-wide significant variants but revealed suggestive signals near ASAP1, EIF2AK2, and FOXP1, indicating a polygenic and ecotype-specific architecture. Overlapping candidate genes across analyses included TH (common to all) and EIF2AK2 (present in all ecotypes except FORO). Quantitative-trait analyses detected a single significant SNP within CACNB4 for back length, but none for the other traits. Overall, reduced body size in Eritrean IC appears to be a complex trait controlled by multiple loci, involving both conserved growth regulators and genes related to metabolic efficiency and environmental adaptation. These findings provide a genomic basis for future breeding strategies to improve productivity, resilience and sustainability of village poultry production systems in resource-limited regions of Eritrea. - Source: PubMed
Publication date: 2026/07/27
Habteslasie Hortuma APerini FrancescoNgeno KiplangatColombi DanieleLasagna EmilianoDessie TadelleKahi Alexander - Breast cancer is one of the leading causes of cancer-related deaths among women worldwide, with estrogen receptor-positive (ER+) breast cancer being the most common subtype. Cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) have become a crucial therapeutic approach for this type of cancer. However, ER+ breast cancer frequently develops resistance to CDK4/6i, limiting therapeutic efficacy. Alternative splicing is a key post-transcriptional regulatory mechanism that may drive such resistance. In this review, we comprehensively analyzed the literature on the molecular mechanisms and key signaling pathways associated with CDK4/6i resistance in ER+ breast cancer and introduced the role of alternative splicing, with a particular focus on its function in tumor drug resistance. Available evidence suggests that splicing dysregulation may influence resistance through multiple pathways, including cell-cycle control, epithelial-mesenchymal transition, growth factor and RAS/MAPK signaling, and immune-related programs. Recent work has also suggested that reduced expression of the splicing regulator NSRP1 may be associated with CDK4/6i resistance through altered NSD2 splicing and activation of interferon signaling, although this mechanism currently requires further independent validation. Collectively, these findings support alternative splicing as a promising but still evolving area of investigation in CDK4/6i resistance. This work provides deeper insights into the role of alternative splicing in CDK4/6i resistance and offers a theoretical foundation for developing novel therapeutic approaches. Future research may focus on developing drugs that precisely modulate specific splicing events or combining CDK4/6i with splicing modulators to reverse or delay resistance. - Source: PubMed
Cui YuqiuXie JiaCai JialeSi YueHuang HairongYu ShiyiSun Haibo - We investigated the potential of miR-640 to downregulate CDK4/6 inhibitor resistance-associated genes and evaluated its apoptotic, anti-metastatic and anti-proliferative effects, both alone and in combination with abemaciclib in breast cancer cells. miR-640 was identified via GSE126125 dataset analysis. Targets were predicted using miRDB, TargetScan and TargetMiner, filtering for resistance-associated genes. MTT assays determined IC50 values for abemaciclib and combinations. Functional effects were evaluated in MCF7 and MDA-MB-231 cells through Annexin V, cell cycle and wound healing assays. Target gene expression was quantified by RT-qPCR. Successful transfection significantly upregulated miR-640 (~50-fold). The miR-640/abemaciclib combination strongly inhibited migration, induced apoptosis and triggered cell line-specific phase arrests (S and G2/M in MCF7; G0/G1 in MDA-MB-231). Gene expression analysis showed significant downregulation of a comprehensive resistance network (including CDK4/6, CDKN2B, WNT7B, MAP3K1 and AURKA) in MCF7 cells. In MDA-MB-231 cells, PDK1, CDK6, CDKN2B, SMAD2, ZFP91, MAP3K1 and AURKA were significantly suppressed. This study identifies miR-640 as a potent tumour suppressor that resensitises breast cancer cells to CDK4/6 inhibition. By post-transcriptionally downregulating key resistance genes, miR-640-alone or additively with abemaciclib-suppresses proliferation and migration while inducing apoptosis, emerging as a promising combinatorial therapeutic strategy. - Source: PubMed
Alkac Ismail MertBiray Avci Cigir - Despite therapeutic advances in the early-stage triple negative breast cancer (TNBC) setting, residual disease (RD) following neoadjuvant therapy remains a key predictor of a worse prognosis and is a major obstacle to improving patient outcomes. - Source: PubMed
Publication date: 2026/08/04
Rädler Patrick DFelsheim Brooke MFernandez-Martinez AranzazuPfefferle Adam DHayward Michele CSingh BaljitSikov WilliamCarey Lisa APerou Charles M