The COOH terminus of p18INK4C distinguishes function from p16INK4A

Cancer Research

Volumn 61, Issue 10, 2001, Pages 3863-3868

  Gump, J ^a   Turner, S ^a   Koh, J ^a  

^a UNIVERSITY OF VERMONT   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CHIMERIC PROTEIN; CYCLIN DEPENDENT KINASE INHIBITOR; PROTEIN P16; PROTEIN P185;

ACUTE LYMPHOCYTIC LEUKEMIA; ARTICLE; CANCER CELL CULTURE; CARBOXY TERMINAL SEQUENCE; CELL CYCLE; GENE MUTATION; GENE OVEREXPRESSION; HUMAN; HUMAN CELL; PRIORITY JOURNAL; REGULATORY MECHANISM; T CELL LEUKEMIA;

AMINO ACID SEQUENCE; BINDING SITES; CARRIER PROTEINS; CELL CYCLE; CELL CYCLE PROTEINS; CYCLIN-DEPENDENT KINASE INHIBITOR P16; CYCLIN-DEPENDENT KINASE INHIBITOR P18; ENZYME INHIBITORS; HUMANS; LEUKEMIA, T-CELL, ACUTE; MOLECULAR SEQUENCE DATA; PROTEIN STRUCTURE, TERTIARY; SEQUENCE HOMOLOGY, AMINO ACID; STRUCTURE-ACTIVITY RELATIONSHIP; TUMOR CELLS, CULTURED; TUMOR SUPPRESSOR PROTEINS;

EID: 0035872465     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (27)

1. 1-phase progression
2. The hallmarks of cancer
3. Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function
4. Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6
5. Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition
6. A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4
7. A cell cycle regulator potentially involved in genesis of many tumor types
8. Absence of p18 mutations or deletions in lymphoid malignancies
9. The INK4 family of CDK inhibitors
10. Cyclin-dependent kinase inhibitors and human cancer
11. The prognostic significance of altered cyclin-dependent kinase inhibitors in human cancer
12. Role of the cyclin-dependent kinase inhibitors in the development of cancer
13. Inactivation of cyclin-dependent kinase inhibitor genes and development of human acute leukemias
14. Cyclin D-CDK subunit arrangement is dependent on the availability of competing INK4 and p21 class inhibitors
15. Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1), and p27KIP1 in inducing cell cycle arrest, apoptosis, and inhibition of tumorigenicity
16. Structural basis for inhibition of the cyclin-dependent kinase Cdk6 by the tumour suppressor p16INK4a
17. Tumor suppressor INK4: Quantitative structure-function analyses of p18INK4C as an inhibitor of cyclin-dependent kinase 4
18. Structural basis of inhibition of CDK-cyclin complexes by INK4 inhibitors
19. Biologic and biochemical analyses of p16(INK4a) mutations from primary tumors
20. Tumor suppressor p16INK4A: Determination of solution structure and analyses of its interaction with cyclin-dependent kinase 4
21. Tumor suppressor INK4: Determination of the solution structure of p18INK4C and demonstration of the functional significance of loops in p18INK4C and p16INK4A
22. The retinoblastoma protein is phosphorylated during specific phases of the cell cycle
23. Lack of cyclin D-Cdk complexes in Rb-negative cells correlates with high levels of p16INK4/MTS1 tumour suppressor gene product
24. Distinct versus redundant properties among members of the INK4 family of cyclin-dependent kinase inhibitors
25. Regulation of cyclin-dependent kinase 4 during adipogenesis involves switching of cyclin D subunits and concurrent binding of p18INK4c and p27Kipl
26. Induction of p18INK4c and its predominant association with CDK4 and CDK6 during myogenic differentiation
27. Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts