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
- Nicotine, the principal addictive component of tobacco smoke, has traditionally been regarded as non-carcinogenic. However, accumulating evidence over the past two decades has established nicotine as a significant tumor promoter facilitating cancer initiation, progression, metastasis, and therapeutic resistance. This systematic review examines the molecular mechanisms by which nicotine modulates p53-mediated signaling pathways across four major cancer types: lung, gastric, liver, and cervical cancer. In lung cancer, nicotine activates three distinct pathways (β-ARs/α7-nAChR-PKA-HA-p53-VEGF; α7-nAChR/β-ARs-VEGF-PI3K/AKT/NF-κB-p53; and nAChRs-MMP-9-sE-cad-EGFR/IGF-1R-p53), all converging to inhibit p53 activity and promote proliferation, angiogenesis, and cell survival. In gastric cancer, nicotine engages the β-AR-PKC-ERK1/2-AP-1-COX-2-p53-p21/p27 pathway, suppressing p53-mediated cell cycle arrest. In liver cancer, nicotine acts through the SETDB1-p53-RS-STAT1-CCND1-PI3K/AKT and CDK6-p53-RS-PIN1-STAT1 pathways (enhancing mutant p53-RS gain-of-function) and the β2-AR/PI3K/AKT pathway (suppressing p53 expression). In cervical cancer, nicotine drives malignant progression via the Rps27a-Mdm2-p53-p21 and PI3K/AKT-p53-p21 pathways. Nicotine's impact on p53 is highly context-dependent: it inactivates wild-type p53 while enhancing gain-of-function of mutant p53, particularly p53-RS. This review expands the theoretical framework of nicotine-induced carcinogenesis, highlights concerns regarding alternative nicotine delivery systems and crosstalk between oxidative stress and p53 regulation, and provides a scientific basis for early diagnosis, targeted therapy, and prevention of smoking-related cancers. - Source: PubMed
Publication date: 2026/06/05
Jiang QinhanZhang ZhongweiZhou JianmingZhou TongWang Huai - Cyclin-dependent kinase 6 (CDK6) regulates adipogenesis and beige fat formation, but its role in preadipocyte metabolism is unclear. The mouse embryonic fibroblast cell line 3 T3-L1 is a well-established preadipocyte model with high adipogenic potential under adipogenic stimulation. Here, we employed label-free, non-invasive Raman imaging to investigate the metabolic profile of 3 T3-L1 cells following CDK6 knockout (KO) at the single-cell level. To improve the specificity of spectral interpretation, isolated cellular mitochondria and mouse skin tissue were used as reference standards for mitochondrial and collagen Raman fingerprints, respectively. True component analysis (TCA) was applied to Raman hyperspectral datasets to decompose complex spectral signals into distinct biochemical components with corresponding spatial distributions. Compared to wild-type (WT) cells, CDK6 ablation increased mitochondrial content and the unsaturated-to-saturated fatty acid ratio, but reduced collagen and overall lipid content. These shifts suggest that CDK6 deletion promotes mitochondrial metabolism and suppresses extracellular matrix synthesis, thereby conferring beneficial metabolic changes that support differentiation potential toward beige adipocytes. Four Raman spectral biomarkers (I, I, I, I) enabled effective cell-type discrimination. For hyperspectral data processing, we employed a machine learning-based pipeline comprising preprocessing (baseline correction and normalization), dimensionality reduction via principal component analysis (PCA), and classification using multiple algorithms. Among these, the linear discriminant analysis (LDA) model achieved the highest classification accuracy of 98.3% in discriminating WT and KO cells. This study demonstrates that Raman spectroscopy not only enables label-free analysis of subtle metabolic phenotypes at the single-cell level but also provides a novel platform for predicting adipocyte differentiation fate. - Source: PubMed
Publication date: 2026/05/25
Zhou YixuanXu YuelinCheng SiyaoNi XintaoZhang LuZhang XinHou XiaoliXia Daozong - In RAS-mutant tumors, ERK phosphorylates the mitochondrial fission GTPase DRP1 to promote mitochondrial fission. DRP1 activity is tumor-promoting in pancreatic and other RAS-driven cancers, but its role in therapeutic resistance is unknown. - Source: PubMed
Publication date: 2026/05/22
Sharmin SalmaKashatus Jennifer AAdair Sara JLoewgren Emma BakallFallahi-Sichani MohammadBauer Todd WKashatus David F - Thoracic SMARCA4-deficient undifferentiated tumors (SMARCA4-UT) are rare malignancies characterized by resistance to chemotherapy and poor clinical outcomes. While immunotherapy have shown promise, especially in the first-line treatment, effective therapeutic strategies for patients with PD-L1-negative tumors and complex genomic profiles remain undefined. We report a case of chemorefractory SMARCA4-UT in a patient presenting with cervical mass. CGP revealed pathogenic , , and mutations. Despite PD-L1 negativity, the tumor exhibited TMB-H and a dominant smoking signature. Guided by precision oncology targeting both immunogenic profile and cell-cycle dysregulation, the patient was treated with dual immunotherapy (pembrolizumab plus ipilimumab) combined with the CDK4/6 inhibitor palbociclib. This novel regimen elicited a metabolic partial response within 1.5 months, which has been sustained for over 4 months. To our knowledge, this is the first report demonstrating the efficacy of dual checkpoint blockade plus CDK4/6 inhibition in SMARCA4-UT. This case highlights potential of biomarker-driven therapies to overcome resistance in rare thoracic neoplasms. - Source: PubMed
Publication date: 2026/05/19
Tokat Ünal MetinBilgiç Şevval NurAdibi AshkanAydın EsranurTutar OnurCansız HilalAltay Ali YılmazAkgul Babacan NalanÖzgü EylülManea Alina MelisaDemiray Mutlu - MicroRNAs (miRNAs) are central post-transcriptional regulators that shape oncogenic and tumor-suppressive networks through RNA-induced silencing complex (RISC)-mediated repression of target mRNAs. Among these, hsa-miR-107-a member of the miR-16 family encoded within an intron of the PANK1 gene-has emerged as a particularly paradoxical regulator in cancer. Accumulating evidence indicates that miR-107 cannot be classified as a single-function miRNA; instead, it behaves as a context-dependent "molecular switch" whose impact is dictated by tissue-specific target availability, tumor stage, and the surrounding regulatory landscape. This review synthesizes mechanistic and translational data explaining how miR-107 exerts opposing roles as both a tumor suppressor and an oncomiR. In tumor-suppressive contexts, miR-107 integrates into stress-response circuitry via a p53/PANK1/miR-107 axis, repressing HIF-1β, impairing HIF-1 complex formation, and reducing VEGF-driven angiogenesis. miR-107 also restricts proliferation and invasion by targeting cell-cycle kinases (e.g., CDK6 and CDK8), suppressing NOTCH2 signaling in glioma, and attenuating pro-survival PI3K/AKT signaling indirectly in NSCLC through BDNF repression. Conversely, in aggressive cancers, miR-107 promotes malignancy through "meta-oncogenic" disruption of global miRNA biogenesis by targeting DICER1, enabling EMT programs via loss of miR-200 family activity. It also activates PI3K/AKT signaling through direct repression of PTEN (notably in bladder cancer) and enhances metastatic behavior in colorectal cancer by co-silencing metastasis suppressors such as DAPK and KLF4. A distinctive layer of complexity is added by miR-107-mediated miRNA-miRNA interaction, exemplified by direct destabilization of the tumor-suppressive let-7 family in advanced breast cancer. Therefore, the review highlights higher-order regulation by lncRNA competing endogenous RNA (ceRNA) "sponges" that sequester miR-107 (e.g., LINC00662, UASR1, H19, MFI2-AS1), thereby rewiring downstream oncogenic pathways. We discuss emerging clinical implications of miR-107 as a biomarker and as a therapeutic lever for reversing multidrug resistance, while outlining key challenges for safe, context-aware miRNA-based interventions. - Source: PubMed
Publication date: 2026/06/02
Ragab Mamdouh AFathy NevineAttia Yasmin MAmer Eman AFahim Sally A