CDK6 (phospho-Tyr13) Antibody
- Known as:
- CDK6 (phosphorilated-Tyr13) Antibody
- Catalog number:
- abx000374
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CDK6 (phospho-Tyr13) Antibody
Related genes to: CDK6 (phospho-Tyr13) 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-Tyr13) Antibody
Related articles to: CDK6 (phospho-Tyr13) Antibody
- Senescent cells accumulate following chemotherapy and during aging, where they contribute to dysfunction through the pro-inflammatory arm of the senescence-associated secretory phenotype (SASP), termed NF-κB-associated SASP (NASP). Here we show that short-term inhibition of CDK4/6 with abemaciclib suppresses established NASP in pre-existing senescent cells both in vitro and in vivo. This senomorphic effect reduces the pro-tumorigenic activity of chemotherapy-induced senescent cells and improves physical function in mice following chemotherapy. Genetic knockdown of CDK4/6 phenocopied these effects, confirming a CDK4/6-dependent mechanism. Mechanistically, CDK4/6 inhibition suppressed retinoic acid signaling, and the RARα antagonist agn194310 similarly reduced NASP expression. CDK4 and CDK6 interacted with NF-κB, while CDK4 additionally bound RARα, and these interactions were disrupted by abemaciclib. In aged mice, abemaciclib and agn194310 reduced systemic NASP expression and improved physical performance. Together, these findings identify the CDK4/6-RARα-NF-κB axis as a therapeutic target for senomorphic interventions. - Source: PubMed
Publication date: 2026/07/17
Wang BoshiPiccolantonio AlessioAltulea AbdullahHuang MenglingJoshi TrupthiPagliarin FrancescaDi Palma MicheleLin YaoMackedenski SebastianUstyantsev KirillJager CorineBerezikov EugeneDemaria Marco - Mesenchymal Stem Cells (MSCs) play a pivotal role in regenerative medicine due to their multipotency and immunomodulatory properties. However, during expansion, MSCs undergo senescence, characterized by a decline in proliferation, impairment of differentiation potential, and altered secretory profiles, which limits their therapeutic efficacy. This study aimed to identify novel molecular regulators and network-level interactions underlying MSC senescence through microarray analysis of the GSE7888 dataset, comparing early and senescent MSCs. - Source: PubMed
Sayahpour Forough-AzamNejati MarjanRouhollahi-Masoumi MahyaBaghaban Eslaminejad MohamadrezaTaleahmad Sara - Objective To explore the immune landscape of patients with lung adenocarcinoma with drainage lymph nodes by single-cell sequencing technology. Methods The lung cancer single cell dataset (GSE277742) was obtained from the Gene Expression Omnibus (GEO) database of the National Center for Biotechnology Information (NCBI). The dataset included intrathoracic DLN from 18 patients with pathologically confirmed lymph node metastasis and 4 control patients without evidence of metastasis. R language was used for data quality control, dimensionality reduction clustering, cell subgroup annotation and cell communication analysis to identify key cell subsets and screen differentially expressed genes. Kaplan-Meier survival analysis was performed using the TCGA database. Results Single cell sequencing analysis showed that the proportion of CD8 T cells in patients with draining lymph nodes was significantly higher, among which cyclin-dependent kinase 6(CDK6), cyclin D3(CCND3), CCNH, cyclin-dependent kinase inhibitor 2A/B/D(CDKN2A/B/D) and retinoblastoma transcriptional corepressor 1(RB1) were highly expressed. TCGA database analysis showed that the expression of genes related to the BIOCARTA_CELLCYCLE_PATHWAY pathway was significantly different between tumor and normal samples, and was related to survival. Conclusion Several key genes differentially expressed in the draining lymph nodes of patients with lung adenocarcinoma are screened by bioinformatics methods, which provides a new perspective for further analysis of the regulatory mechanism of the immune microenvironment of lung adenocarcinoma with draining lymph nodes. - Source: PubMed
Shi TingweiLi WenFan ZhiliangLiu HanshenZhao QingYu YilongPu Xiang - In RAS-mutant tumours, ERK phosphorylates the mitochondrial fission GTPase DRP1 to promote mitochondrial fission. DRP1 activity is tumour-promoting in pancreatic and other RAS-driven cancers, but its role in therapeutic resistance is unknown. - Source: PubMed
Publication date: 2026/07/14
Sharmin SalmaKashatus Jennifer AAdair Sara JLoewgren Emma BakallFallahi-Sichani MohammadBauer Todd WKashatus David F - mRNA nuclear export is an essential biological process that is mediated primarily by nuclear export factor 1 (NXF1). NXF1 exerts its mRNA transport activity by binding to adaptor proteins. In an effort to identify novel NXF1 adaptors involved in hepatocellular carcinoma (HCC) development, we discovered that C7orf25, a previously uncharacterized protein named proliferation-associated NXF1 adaptor (PANAD), interacts with NXF1 in the nucleus. Specifically, the R122/E125/G133/D139 residues of PANAD bound to the Q20/K22/K23 residues in the RBD of NXF1. This binding disrupted the intramolecular interaction between the RBD and NTF2L domains of NXF1, thereby enhancing the association of NXF1 with target mRNAs. The mRNAs whose nuclear export was impaired upon PANAD knockdown were highly enriched in cell proliferation pathways. Moreover, PANAD directly bound to CDK6 mRNA. Gain- and loss-of-function analyses in cellular and mouse models revealed that PANAD accelerated G1/S transition and tumor cell proliferation, promoted colony formation and hepatoma xenograft growth, and acted through interactions with NXF1 to increase the nuclear export and translation of mRNAs encoding proliferation stimulators, including CDK6. PANAD and CDK6 were both upregulated in HCC tissues and were positively correlated. Furthermore, PANAD-overexpressing hepatoma cells exhibited increased sensitivity to the CDK4/6 inhibitor palbociclib, whereas PANAD-silenced cells exhibited reduced sensitivity. These findings identify PANAD as a novel NXF1 adaptor; delineate its critical regulatory roles in mRNA nuclear export, G1/S transition and tumor development; and highlight its potential as both a therapeutic target and a predictive biomarker for CDK4/6-targeted therapy. - Source: PubMed
Publication date: 2026/07/15
Liu Jin-YuFeng Huan-HuiXie ChenChen Ya-JingLuo Xiao-YuWang YuChen Zhan-LiZhang QiYang Jin-EZhuang Shi-Mei