Regulation of Mammalian G1 Cyclin Dependent Kinase Complexes by Transforming Growth Factor-ß
Year: 1999
Type: dissertation
Abstract: A 1. Mammalian cell cycle Retinoblastoma/E2F-pathway as a controller of G 1 -progression Control of cell cycle progression by G 1 and G 1 /S specific Cdk-cyclin complexes D-type cyclins The activity of Cdk4 or Cdk6-cyclin D complexes is required for pRb phosphorylation in G 1 E-type cyclins Cdk2-cyclin E-complexes in G 1 /S-phase transition A 2. Regulation of Cdk activity Cdk activity requires cyclin binding and activating phosphorylation Inhibitory tyrosine phosphorylation Cyclin dependent kinase inhibitors p21 familyStructural motifs of p21 family The p21 family members are both negative and positive regulators of the Cdk-activity p27 Kip p27 in cellular differentiation and tumorigenesis p21 CIP1,WAF1,Sdi1 and p57 Kip p16 family Structural motifs of the p16 family p16 INK4A,MTS1 acts in pRb pathway p15 INK4B, MTS2 is regulated by TGF-β p16 and p15 loci as tumor suppressors p18 INK4C and p19 INK4D24 A 3. Transforming growth factor-β TGF-β signal transduction TGF-β as a growth inducer Growth inhibitory effects of TGF-β mediated by cell cycle machinery proteins pRb as a mediator of TGF-β growth inhibitory signal Cdk inhibitors as mediators of TGF-β growth arrest Co-operation between p15 and p27 in TGF-β growth arrest p21 mediates TGF-β growth arrest in some cell types Viral oncoproteins prevent TGF-β growth arrest by binding to Cdkis The effects of TGF-β on Cdk and cyclin subunits A 4. Hepatocyte growth factor A 5. Ras oncogene as a cellular growth regulator B. AIMS OF THE PRESENT STUDY
Source: Työväentutkimus Vuosikirja
Author: Minna Taipale
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1624924943