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Primary antibodies against PARP, Bd-2, Bax, cydin D1, cyclin-dependent kinase (CDK) 4, CDK6, IRE1[alpha], p-eIF21[alpha], Bip, and GAPDH, together with the secondary antibodies, were obtained from Cell Signaling Technology, Inc.
Candidate target genes of hsa-miR-424-5p and hsa-miR-377 Gene name Main pathway Target Accession gene ID hsa-miR-424-5p Hypoxia and angiogenesis HIF1A MIRT005926 CUL2 MIRT005927 Cell cycle CDK6 MIRT000938 CCND1 MIRT000941 CCNE1 MIRT000936 CCND3 MIRT000937 hsa-miR-377 MAPK pathway PPM1A MIRT000990 PI3K-akt pathway PAK1 MIRT000991 HIF1A: Hypoxia-inducible factor 1A; CUL2: Cullin 2; CDK: Cyclin-dependent kinase; CCND1: Cyclin D1; CCNE1: Cyclin E1; CCND3: Cyclin D3; MAPK: Mitogen-activated protein kinase; PPM1A: Protein phosphatase magnesium-dependent 1A; PI3K: Phosphatidyl inositol 3'-kinase; PAK1: p21-activated kinase 1.
At the molecular level, the inhibition of proliferation was associated with significantly reduced CDK6 expression and an increased level of p27 in ER+ cells but not in ER-cells, whereas a common feature in all cell lines was significantly decreased retinoblastoma protein phosphorylation.
The transition through G1 to S phase is regulated by cyclins, cyclin-dependent kinases (CDK)-CDK4 and CDK6 and their inhibitors.
Tambien, se hicieron pruebas con anticuerpos contra EGFR, p53, CDK6, PTEN y p21.
Some CDKs, such as CDK1-CDK4, CDK6 and perhaps CDK11, are involved in progression through the cell cycle, whereas CDK7 has dual roles as a CDK-activating kinase (CAK) and a regulator of the transcriptional machinery.
Indianapolis, Indiana-based global pharmaceuticals specialist Eli Lilly and Company's (NYSE: LLY) Phase 3 JUNIPER study evaluating Verzenio (abemaciclib), a cyclin-dependent kinase 4 and CDK6 inhibitor, as monotherapy in KRAS-mutated, advanced non-small lung cancer (NSCLC) did not meet its primary endpoint of overall survival (OS), the company said.
The two cell-cycle kinases CDK4 and CDK6 normally facilitate cell-cycle progression but are abnormally activated in certain cancers.
As to the mechanisms, levels of inactive or phosphorylated (p) p53, p21, CDK6, CDK4, cyclin Dl, and E2F1 were immunodetected.
2] Human genes: EGFR, epidermal growth factor receptor; KRAS, kirsten rat sarcoma viral oncogene homolog; ERBB2, v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2; EML4, echinoderm microtubule-associated protein like 4; ALK, anaplastic lymphoma receptor tyrosine kinase; SEPT9, septin 9; CDKN2A, cyclin-dependent kinase inhibitor 2A; MET, MET proto-oncogene, receptor tyrosine kinase; CDK6, cyclin-dependent kinase 6; BRAF, B-Raf proto-oncogene, serine/threonine kinase.
Kip1) cell cycle 2006 progression 8 CDK6 Probably involved in Chilosi et al.
Induction of p18INK4c and its predominant association with CDK4 and CDK6 during myogenic differentiation.
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- CDK2-associated dual specificity phosphatase
- CDK2-associated dual-specificity phosphatase
- CDK4 gene
- CDK4 gene
- CDK4 inhibitor p16-INK4, INK4a
- CDK4B inhibitor
- CDK5-Binding Protein
- CDK6 inhibitor p18
- CDK8 protein kinase
- CDK8-like cyclin-dependent kinase
- CDK9-associated C-type protein