Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK050118-07
Application #
6689530
Study Section
General Medicine B Study Section (GMB)
Program Officer
Wilder, Elizabeth L
Project Start
1997-06-10
Project End
2007-11-30
Budget Start
2003-12-01
Budget End
2004-11-30
Support Year
7
Fiscal Year
2004
Total Cost
$344,352
Indirect Cost

  Institution

Name
Children's Hospital Boston
Department
Type
DUNS #
076593722
City
Boston
State
MA
Country
United States
Zip Code
02115

  Publications

Qin, Shan; Taglienti, Mary; Cai, Lei et al. (2012) c-Met and NF-ýýB-dependent overexpression of Wnt7a and -7b and Pax2 promotes cystogenesis in polycystic kidney disease. J Am Soc Nephrol 23:1309-18
Qin, Shan; Taglienti, Mary; Nauli, Surya M et al. (2010) Failure to ubiquitinate c-Met leads to hyperactivation of mTOR signaling in a mouse model of autosomal dominant polycystic kidney disease. J Clin Invest 120:3617-28
Liu, Yingjie; Chattopadhyay, Nibedita; Qin, Shan et al. (2009) Coordinate integrin and c-Met signaling regulate Wnt gene expression during epithelial morphogenesis. Development 136:843-53
Natoli, Thomas A; Alberta, Julia A; Bortvin, Alex et al. (2004) Wt1 functions in the development of germ cells in addition to somatic cell lineages of the testis. Dev Biol 268:429-40
Zhang, Hong; Palmer, Rachel; Gao, Xiaobo et al. (2003) Transcriptional activation of placental growth factor by the forkhead/winged helix transcription factor FoxD1. Curr Biol 13:1625-9
Natoli, Thomas A; McDonald, Alice; Alberta, Julia A et al. (2002) A mammal-specific exon of WT1 is not required for development or fertility. Mol Cell Biol 22:4433-8
Natoli, Thomas A; Liu, Jing; Eremina, Vera et al. (2002) A mutant form of the Wilms' tumor suppressor gene WT1 observed in Denys-Drash syndrome interferes with glomerular capillary development. J Am Soc Nephrol 13:2058-67