Ablation of a peptidyl prolyl isomerase Pin1 from p53-null mice accelerated thymic hyperplasia by increasing the level of the intracellular form of Notch1

Oncogene

Volumn 26, Issue 26, 2007, Pages 3835-3845

  Takahashi, K ^a,b   Akiyama, H ^a   Shimazaki, K ^b   Uchida, C ^a,c   Akiyama Okunuki, H ^b   Tomita, M ^b   Fukumoto, M ^a   Uchida, T ^a  

^a TOHOKU UNIVERSITY   (Japan)

^b SHOWA UNIVERSITY   (Japan)

^c IBARAKI UNIVERSITY   (Japan)

Author keywords

Hyperplasia; Notch1; p53; Presenilin 1; Thymocytes

Indexed keywords

NOTCH1 RECEPTOR; PEPTIDYLPROLYL ISOMERASE PIN1; PROTEASOME; PROTEIN P53;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CD4+ T LYMPHOCYTE; CD8+ T LYMPHOCYTE; CELL DIFFERENTIATION; CELL INFILTRATION; CONTROLLED STUDY; FEMALE; KIDNEY; LIVER; LUNG INFILTRATE; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEGRADATION; PROTEIN FUNCTION; PROTEIN PROTEIN INTERACTION; THYMOCYTE; THYMUS HYPERPLASIA; THYMUS LYMPHOMA; WILD TYPE;

ANIMALS; BLOTTING, WESTERN; FEMALE; FLOW CYTOMETRY; INTRACELLULAR FLUID; MALE; MICE; MICE, KNOCKOUT; PEPTIDYLPROLYL ISOMERASE; PRESENILIN-1; RECEPTOR, NOTCH1; T-LYMPHOCYTES; THYMUS HYPERPLASIA; TUMOR SUPPRESSOR PROTEIN P53;

MUS;

EID: 34249948703     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/sj.onc.1210153     Document Type: Article

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