Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
about
Trial Watch: Targeting ATM-CHK2 and ATR-CHK1 pathways for anticancer therapyCheckpoint kinase 1 in DNA damage response and cell cycle regulationRoles of Chk1 in cell biology and cancer therapyChk1 targeting reactivates PP2A tumor suppressor activity in cancer cellsOncogenic stress sensitizes murine cancers to hypomorphic suppression of ATRTelomere Replication Stress Induced by POT1 Inactivation Accelerates Tumorigenesis.Is activation of the intra-S checkpoint in human fibroblasts an important factor in protection against UV-induced mutagenesis?Cell cycle proteins as promising targets in cancer therapyImpact of Age and Insulin-Like Growth Factor-1 on DNA Damage Responses in UV-Irradiated Human Skin.CRL4(CDT2) targets CHK1 for PCNA-independent destruction.Wnt-driven intestinal tumourigenesis is suppressed by Chk1 deficiency but enhanced by conditional haploinsufficiency.Insulin-like Growth Factor 1 Receptor Signaling Is Required for Optimal ATR-CHK1 Kinase Signaling in Ultraviolet B (UVB)-irradiated Human Keratinocytes.Checkpoint kinase 1 is essential for normal B cell development and lymphomagenesis.Chk1 is essential for the development of murine epidermal melanocytes.
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Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
description
2011 nî lūn-bûn
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2011年の論文
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年學術文章
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2011年學術文章
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name
Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
@en
Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
@nl
type
label
Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
@en
Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
@nl
prefLabel
Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
@en
Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis.
@nl
P2860
P50
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Chk1 is essential for chemical carcinogen-induced mouse skin tumorigenesis
@en
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10.1038/ONC.2011.326
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2011-08-01T00:00:00Z