The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest.

The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Research Abstract Details 

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The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Abstract Text:

Steven J Wall,Zhi-Duan Zhong,Yves A DeClerck,

The extracellular matrix is a crucial component in determining cell fate. Fibrillar collagen in its native form inhibits cell proliferation, whereas in its monomeric form it stimulates proliferation. The observation of elevated levels of p27(KIP1) in cells plated in the presence of fibrillar collagen has led to the assumption that this kinase inhibitor was responsible for cell cycle arrest on fibrillar collagen. Here we provide evidence that p15(INK4b), rather than p27(KIP1), is the cyclin-dependent kinase inhibitor responsible for G0/G1 arrest of human melanoma cells grown on fibrillar collagen. Additionally, we demonstrate that fibrillar collagen can also arrest cells at the G2 phase, which is mediated in part by p21(CIP1). Our data, in addition to identifying cyclin-dependent kinase inhibitors important in cell cycle arrest mediated by fibrillar collagen, demonstrate the complexity of cell cycle regulation and indicate that modulating a single cyclin-dependent kinase inhibitor does not disrupt cell proliferation in the presence of fibrillar collagen.

The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Publishing Authors By Initials

SJ Wall,ZD Zhong,YA DeClerck,

For similar neoplasms: neoplasms by histologic type: neoplasms, germ cell and embryonal: neuroectodermal tumors: neuroendocrine tumors: melanoma research abstracts see: neoplasms: neoplasms by histologic type: neoplasms, germ cell and embryonal: neuroectodermal tumors: neuroendocrine tumors: melanoma research

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The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 24471-6

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 6

MONTH: 06

YEAR: 2007

The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985121

The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Keywords Mesh Terms:

KEYWORDS: Melanoma

MESH TERMS: pathology

Chemical & Substance for Abstract: The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest. Information

Substance Name: Cyclin-Dependent Kinase Inhibitor p27

Registry Number: 147604-94-2

Grant and Affiliation Information for The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest.

AFFILIATION: Division of Hematology-Oncology and Department of Pediatrics, University of Southern California and the Saban Research Institute of the Childrens Hospital Los Angeles, Los Angeles, California 90027, USA.

Country: United States

AGENCY: United States NCI

GRANT: R01 CA98469

ACRONYM: CA

MEDLINETA: J Biol Chem

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