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Articles by J Lazar
Total Records ( 2 ) for J Lazar
  Temple The MGC Project Team , D. S Gerhard , R Rasooly , E. A Feingold , P. J Good , C Robinson , A Mandich , J. G Derge , J Lewis , D Shoaf , F. S Collins , W Jang , L Wagner , C. M Shenmen , L Misquitta , C. F Schaefer , K. H Buetow , T. I Bonner , L Yankie , M Ward , L Phan , A Astashyn , G Brown , C Farrell , J Hart , M Landrum , B. L Maidak , M Murphy , T Murphy , B Rajput , L Riddick , D Webb , J Weber , W Wu , K. D Pruitt , D Maglott , A Siepel , B Brejova , M Diekhans , R Harte , R Baertsch , J Kent , D Haussler , M Brent , L Langton , C. L.G Comstock , M Stevens , C Wei , M. J van Baren , K Salehi Ashtiani , R. R Murray , L Ghamsari , E Mello , C Lin , C Pennacchio , K Schreiber , N Shapiro , A Marsh , E Pardes , T Moore , A Lebeau , M Muratet , B Simmons , D Kloske , S Sieja , J Hudson , P Sethupathy , M Brownstein , N Bhat , J Lazar , H Jacob , C. E Gruber , M. R Smith , J McPherson , A. M Garcia , P. H Gunaratne , J Wu , D Muzny , R. A Gibbs , A. C Young , G. G Bouffard , R. W Blakesley , J Mullikin , E. D Green , M. C Dickson , A. C Rodriguez , J Grimwood , J Schmutz , R. M Myers , M Hirst , T Zeng , K Tse , M Moksa , M Deng , K Ma , D Mah , J Pang , G Taylor , E Chuah , A Deng , K Fichter , A Go , S Lee , J Wang , M Griffith , R Morin , R. A Moore , M Mayo , S Munro , S Wagner , S. J.M Jones , R. A Holt , M. A Marra , S Lu , S Yang , J Hartigan , M Graf , R Wagner , S Letovksy , J. C Pulido , K Robison , D Esposito , J Hartley , V. E Wall , R. F Hopkins , O Ohara and S. Wiemann
 

Since its start, the Mammalian Gene Collection (MGC) has sought to provide at least one full-protein-coding sequence cDNA clone for every human and mouse gene with a RefSeq transcript, and at least 6200 rat genes. The MGC cloning effort initially relied on random expressed sequence tag screening of cDNA libraries. Here, we summarize our recent progress using directed RT-PCR cloning and DNA synthesis. The MGC now contains clones with the entire protein-coding sequence for 92% of human and 89% of mouse genes with curated RefSeq (NM-accession) transcripts, and for 97% of human and 96% of mouse genes with curated RefSeq transcripts that have one or more PubMed publications, in addition to clones for more than 6300 rat genes. These high-quality MGC clones and their sequences are accessible without restriction to researchers worldwide.

  L Lu , P Li , C Yang , T Kurth , M Misale , M Skelton , C Moreno , R. J Roman , A. S Greene , H. J Jacob , J Lazar , M Liang and A. W. Cowley
 

Chromosome 13 consomic and congenic rat strains were analyzed to investigate the pattern of genomic pathway utilization involved in protection against salt-sensitive hypertension and renal injury. Introgression of the entire Brown-Norway chromosome 13 (consomic SS-13BN) or nonoverlapping segments of this chromosome (congenic strains, 16 Mbp in D13Rat151–D13Rat197 or 14 Mbp in D13Rat111–D13Got22) into the genome of the Dahl salt-sensitive rat attenuated salt-induced hypertension and proteinuria. mRNA abundance profiles in the renal cortex and the renal medulla from rats receiving 0.4% or 8% NaCl diets revealed two important features of pathway recruitment in these rat strains. First, the two congenic strains shared alterations in several pathways compared with Dahl salt-sensitive rats, despite the fact that the genomic segments introgressed in the two congenic strains did not overlap. Second, even though the genomic segment introgressed in each congenic strain was a part of the chromosome introgressed in the consomic strain, pathways altered in each congenic strain were not simply a subset of those altered in the consomic. Supporting the relevance of the mRNA data, differential expression of oxidative stress-related genes among the four strains of rats was associated with differences in urinary excretion of lipid peroxidation products. The findings suggest that different genetic alterations might converge to influence shared pathways in protection from hypertension, and that, depending on the genomic context, the same genetic alteration might diverge to affect different pathways.

 
 
 
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