A marked deficiency in circulating and renal IGF-I peptide does not inhibit compensatory renal enlargement in uninephrectomized mice

Growth Hormone and IGF Research

Volumn 21, Issue 5, 2011, Pages 279-284

  Landau, Daniel ^a   Biada, Jaclyn ^c   Chen, Yu ^b   Sood, Sumita ^b   Yakar, Shoshanah ^d   LeRoith, Derek ^d   Segev, Yael ^a   Rabkin, Ralph ^b,c  

^a BEN GURION UNIVERSITY OF THE NEGEV   (Israel)

^b STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c VA PALO ALTO HEALTH CARE SYSTEM   (United States)

^d MOUNT SINAI SCHOOL OF MEDICINE   (United States)

Author keywords

Animal; Gene disruption; Insulin like growth factor I; Knockout; Mice; Models; Renal hypertrophy; Uninephrectomy

Indexed keywords

MESSENGER RNA; SOMATOMEDIN C; SOMATOMEDIN C RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DEVELOPMENTAL DISORDER; DISEASE SEVERITY; DOWN REGULATION; KIDNEY HYPERTROPHY; KIDNEY SIZE; MALE; MEDIATOR RELEASE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DETERMINATION; PROTEIN FUNCTION; PROTEIN PHOSPHORYLATION; PROTEIN SYNTHESIS; STRAIN DIFFERENCE; UPREGULATION;

ANIMALS; ANIMALS, GENETICALLY MODIFIED; BLOTTING, WESTERN; INSULIN-LIKE GROWTH FACTOR I; KIDNEY; MALE; MICE; NEPHRECTOMY; ORGAN SIZE; POLYMERASE CHAIN REACTION;

EID: 80052558195     PISSN: 10966374     EISSN: 15322238     Source Type: Journal    
DOI: 10.1016/j.ghir.2011.07.008     Document Type: Article

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