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10.1161/HYPERTENSIONAHA.114.04736 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.114.04736 C4412596!4412596 !25776069     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25776069 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mutation of SH2B3 (LNK), a genome-wide association study candidate for hypertension, attenuates Dahl salt-sensitive hypertension via inflammatory modulation |pdf=|usr=}}{{25776069 }} gab.com Text Mutation of SH2B3 (LNK), a genome-wide association study candidate for hypertension, attenuates Dahl salt-sensitive hypertension via inflammatory modulation JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25776069 #FOAvip Human genome-wide association studies have linked SH2B adaptor protein 3 (SH2B3, LNK) to hypertension and renal disease, although little experimental investigation has been performed to verify a role for SH2B3 in these pathologies. SH2B3, a member of the SH2B adaptor protein family, is an intracellular adaptor protein that functions as a negative regulator in many signaling pathways, including inflammatory signaling processes. To explore a mechanistic link between SH2B3 and hypertension, we targeted the SH2B3 gene for mutation on the Dahl salt-sensitive (SS) rat genetic background with zinc-finger nucleases. The resulting mutation was a 6-bp, in-frame deletion within a highly conserved region of the Src homology 2 (SH2) domain of SH2B3. This mutation significantly attenuated Dahl SS hypertension and renal disease. Also, infiltration of leukocytes into the kidneys, a key mediator of Dahl SS pathology, was significantly blunted in the Sh2b3(em1Mcwi) mutant rats. To determine whether this was because of differences in immune signaling, bone marrow transplant studies were performed in which Dahl SS and Sh2b3(em1Mcwi) mutants underwent total body irradiation and were then transplanted with Dahl SS or Sh2b3(em1Mcwi) mutant bone marrow. Rats that received Sh2b3(em1Mcwi) mutant bone marrow had a significant reduction in mean arterial pressure and kidney injury when placed on a high salt diet (4% NaCl). These data further support a role for the immune system as a modulator of disease severity in the pathogenesis of hypertension and provide insight into inflammatory mechanisms at play in human hypertension and renal disease. Twit Text FOAVip Mutation of SH2B3 (LNK), a genome-wide association study candidate for hypertension, attenuates Dahl salt-sensitive hypertension via inflammatory modulation ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25776069 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25776069 #FOAvip English Wikipedia <ref>{{Cite pmid|25776069 }}</ref> Mutation of SH2B3 (LNK), a genome-wide association study candidate for hypertension, attenuates Dahl salt-sensitive hypertension via inflammatory modulation #MMPMID25776069 Rudemiller NP ; Lund H ; Priestley JR ; Endres BT ; Prokop JW ; Jacob HJ ; Geurts AM ; Cohen EP ; Mattson DL Hypertension 2015[May]; 65 (5 ): 1111-7 PMID25776069 show ga Human genome-wide association studies have linked SH2B adaptor protein 3 (SH2B3, LNK) to hypertension and renal disease, although little experimental investigation has been performed to verify a role for SH2B3 in these pathologies. SH2B3, a member of the SH2B adaptor protein family, is an intracellular adaptor protein that functions as a negative regulator in many signaling pathways, including inflammatory signaling processes. To explore a mechanistic link between SH2B3 and hypertension, we targeted the SH2B3 gene for mutation on the Dahl salt-sensitive (SS) rat genetic background with zinc-finger nucleases. The resulting mutation was a 6-bp, in-frame deletion within a highly conserved region of the Src homology 2 (SH2) domain of SH2B3. This mutation significantly attenuated Dahl SS hypertension and renal disease. Also, infiltration of leukocytes into the kidneys, a key mediator of Dahl SS pathology, was significantly blunted in the Sh2b3(em1Mcwi) mutant rats. To determine whether this was because of differences in immune signaling, bone marrow transplant studies were performed in which Dahl SS and Sh2b3(em1Mcwi) mutants underwent total body irradiation and were then transplanted with Dahl SS or Sh2b3(em1Mcwi) mutant bone marrow. Rats that received Sh2b3(em1Mcwi) mutant bone marrow had a significant reduction in mean arterial pressure and kidney injury when placed on a high salt diet (4% NaCl). These data further support a role for the immune system as a modulator of disease severity in the pathogenesis of hypertension and provide insight into inflammatory mechanisms at play in human hypertension and renal disease. |*Mutation [MESH] |Adaptor Proteins, Signal Transducing [MESH] |Animals [MESH] |Blood Pressure [MESH] |DNA/*genetics [MESH] |Electrophoresis, Polyacrylamide Gel [MESH] |Genome-Wide Association Study [MESH] |Hypertension/*genetics/immunology/metabolism [MESH] |Immunity, Cellular [MESH] |Inflammation/*genetics/immunology/metabolism [MESH] |Kidney/metabolism/pathology [MESH] |Proteins/*genetics/metabolism [MESH] |Rats [MESH] |Rats, Inbred Dahl [MESH] |Rats, Mutant Strains [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Signal Transduction [MESH]Mutation of SH2B3 (LNK), a genome-wide association study candidate for(epmc).pdf DeepDyve Pubget Overpricing