Should SIX2 be routinely tested in patients with isolated congenital abnormalities of kidneys and/or urinary tract (CAKUT)?
暂无分享,去创建一个
[1] R. Salomon,et al. Spectrum of HNF1B mutations in a large cohort of patients who harbor renal diseases. , 2010, Clinical journal of the American Society of Nephrology : CJASN.
[2] S. Parodi,et al. Renal outcome in patients with congenital anomalies of the kidney and urinary tract. , 2009, Kidney international.
[3] A. Bakkaloğlu,et al. SIX2 and BMP4 mutations associate with anomalous kidney development. , 2008, Journal of the American Society of Nephrology : JASN.
[4] A. Schedl. Renal abnormalities and their developmental origin , 2007, Nature Reviews Genetics.
[5] G. Dressler,et al. Six2 is required for suppression of nephrogenesis and progenitor renewal in the developing kidney , 2006, The EMBO journal.
[6] R. Salomon,et al. Prevalence of mutations in renal developmental genes in children with renal hypodysplasia: results of the ESCAPE study. , 2006, Journal of the American Society of Nephrology : JASN.
[7] J. Groothoff,et al. Etiology and epidemiology of end-stage renal disease in Dutch children 1987–2001 , 2005, Pediatric Nephrology.
[8] C. Englert,et al. The transcription factor Six2 activates expression of the Gdnf gene as well as its own promoter , 2004, Mechanisms of Development.
[9] K. Ikeda,et al. Molecular Interaction and Synergistic Activation of a Promoter by Six, Eya, and Dach Proteins Mediated through CREB Binding Protein , 2002, Molecular and Cellular Biology.
[10] A. Streit. Extensive cell movements accompany formation of the otic placode. , 2002, Developmental biology.
[11] B. Fivush,et al. Chronic renal insufficiency in children and adolescents: the 1996 annual report of NAPRTCS , 1998, Pediatric Nephrology.
[12] T. Saito,et al. Tissue and developmental distribution of Six family gene products. , 1998, The International journal of developmental biology.