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10.1016/j.cub.2005.02.050 http://scihub22266oqcxt.onion/10.1016/j.cub.2005.02.050 15823540!ä!15823540 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Biol 2005 ; 15 (7): 667-71 Nephropedia Template TP {{tp|p=15823540|t=2005. Defective skeletogenesis with kidney stone formation in dwarf zebrafish mutant for trpm7 |pdf=|usr=}}{{15823540}} gab.com Text Defective skeletogenesis with kidney stone formation in dwarf zebrafish mutant for trpm7 JO: Curr Biol http://www.kidney.de/pget.php?&tw=1&pmid=15823540 #FOAvip Development of the adult form requires coordinated growth and patterning of multiple traits in response to local gene activity as well as to global endocrine and physiological effectors. An excellent example of such coordination is the skeleton. Skeletal development depends on the differentiation and morphogenesis of multiple cell types to generate elements with distinct forms and functions throughout the body. We show that zebrafish touchtone/nutria mutants exhibit severe growth retardation and gross alterations in skeletal development in addition to embryonic melanophore and touch-response defects. These alterations include accelerated endochondral ossification but delayed intramembranous ossification, as well as skeletal deformities. We show that the touchtone/nutria phenotype results from mutations in trpm7, which encodes a transient receptor potential (TRP) family member that functions as both a cation channel and kinase. We find trpm7 expression in the mesonephric kidney and show that mutants develop kidney stones, indicating renal dysfunction. These results identify a requirement for trpm7 in growth and skeletogenesis and highlight the potential of forward genetic approaches to uncover physiological mechanisms contributing to the development of adult form. Twit Text FOAVip Defective skeletogenesis with kidney stone formation in dwarf zebrafish mutant for trpm7 ????Curr Biol http://www.kidney.de/pget.php?&tw=1&pmid=15823540 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15823540 #FOAvip English Wikipedia <ref>{{Cite pmid|15823540}}</ref> Defective skeletogenesis with kidney stone formation in dwarf zebrafish mutant for trpm7 #MMPMID15823540 Elizondo MR; Arduini BL; Paulsen J; MacDonald EL; Sabel JL; Henion PD; Cornell RA; Parichy DM Curr Biol 2005[Apr]; 15 (7): 667-71 PMID15823540show ga Development of the adult form requires coordinated growth and patterning of multiple traits in response to local gene activity as well as to global endocrine and physiological effectors. An excellent example of such coordination is the skeleton. Skeletal development depends on the differentiation and morphogenesis of multiple cell types to generate elements with distinct forms and functions throughout the body. We show that zebrafish touchtone/nutria mutants exhibit severe growth retardation and gross alterations in skeletal development in addition to embryonic melanophore and touch-response defects. These alterations include accelerated endochondral ossification but delayed intramembranous ossification, as well as skeletal deformities. We show that the touchtone/nutria phenotype results from mutations in trpm7, which encodes a transient receptor potential (TRP) family member that functions as both a cation channel and kinase. We find trpm7 expression in the mesonephric kidney and show that mutants develop kidney stones, indicating renal dysfunction. These results identify a requirement for trpm7 in growth and skeletogenesis and highlight the potential of forward genetic approaches to uncover physiological mechanisms contributing to the development of adult form. |*Zebrafish[MESH] |Abnormalities, Multiple/genetics/metabolism[MESH] |Animals[MESH] |Base Sequence[MESH] |Bone and Bones/anatomy & histology[MESH] |Chromosome Mapping[MESH] |DNA, Complementary/genetics[MESH] |Histological Techniques[MESH] |In Situ Hybridization[MESH] |Ion Channels/*genetics/metabolism[MESH] |Kidney Calculi/genetics/*veterinary[MESH] |Kidney/metabolism[MESH] |Larva/metabolism[MESH] |Molecular Sequence Data[MESH] |Osteogenesis/*genetics[MESH] |Protein Kinases/*genetics/metabolism[MESH] |Protein Serine-Threonine Kinases[MESH] |Sequence Analysis, DNA[MESH] |TRPM Cation Channels[MESH]Defective skeletogenesis with kidney stone formation in dwarf zebrafis(epmc).pdf DeepDyve Pubget Overpricing