Pot1b deletion and telomerase haploinsufficiency in mice initiate an ATR-dependent DNA damage response and elicit phenotypes resembling dyskeratosis congenita

Molecular and Cellular Biology

Volumn 29, Issue 1, 2009, Pages 229-240

  He, Hua ^a   Wang, Yang ^a   Guo, Xiaolan ^a   Ramchandani, Sonal ^a   Jin, Ma ^a   Shen, Mei Feng ^a   Garcia, Dennis A ^b   Deng, Yibin ^a   Multani, Asha S ^a   You, Mingjian James ^a   Chang, Sandy ^a,c  

^a Department of Genetics ^*

^b UNIVERSITY OF HOUSTON DOWNTOWN   (United States)

^c UNIVERSITY OF TEXAS MD ANDERSON CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ATR PROTEIN; GENE PRODUCT; GLYCERALDEHYDE 3 PHOSPHATE DEHYDROGENASE; PROTEIN P21; PROTEIN P53; PROTEIN POT1B; TELOMERASE; TUBULIN; UNCLASSIFIED DRUG; ATR PROTEIN, MOUSE; CELL CYCLE PROTEIN; DNA BINDING PROTEIN; POT1B PROTEIN, MOUSE; PROTEIN SERINE THREONINE KINASE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; BONE MARROW DEPRESSION; CELL SURVIVAL; CELL VIABILITY; CHROMOSOMAL INSTABILITY; CHROMOSOME; CONTROLLED STUDY; DNA DAMAGE; DYSKERATOSIS CONGENITA; FEMALE; GENE; GENE DELETION; GENE LOSS; GERM CELL; HEMATOPOIETIC STEM CELL; HYPERPIGMENTATION; IN VITRO STUDY; MALE; MOUSE; NAIL DYSTROPHY; NONHUMAN; PATHOPHYSIOLOGY; PHENOTYPE; POT1B GENE; PRIORITY JOURNAL; TELOMERE; ANIMAL; ANTIBODY SPECIFICITY; BONE MARROW CELL; CELL DEATH; CELL PROLIFERATION; CHEMISTRY; CONFORMATION; CONGENITAL MALFORMATION; ENZYMOLOGY; GENETICS; HAPLOIDY; HEMATOPOIETIC SYSTEM; METABOLISM; MOUSE MUTANT; PATHOLOGY; SURVIVAL;

MUS;

ANIMALS; BONE MARROW CELLS; CELL CYCLE PROTEINS; CELL DEATH; CELL PROLIFERATION; DNA DAMAGE; DNA-BINDING PROTEINS; DYSKERATOSIS CONGENITA; GENE DELETION; HAPLOIDY; HEMATOPOIETIC SYSTEM; MICE; MICE, KNOCKOUT; NUCLEIC ACID CONFORMATION; ORGAN SPECIFICITY; PHENOTYPE; PROTEIN-SERINE-THREONINE KINASES; SURVIVAL ANALYSIS; TELOMERASE; TELOMERE;

EID: 58149467017     PISSN: 02707306     EISSN: None     Source Type: Journal    
DOI: 10.1128/MCB.01400-08     Document Type: Article

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