RGD Reference Report - alpha-Kinase 2 is a novel candidate gene for inherited hypertension in Dahl rats. - Rat Genome Database

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alpha-Kinase 2 is a novel candidate gene for inherited hypertension in Dahl rats.

Authors: Chauvet, C  Crespo, K  Menard, A  Wu, Y  Xiao, C  Blain, M  Roy, J  Deng, AY 
Citation: Chauvet C, etal., J Hypertens. 2011 Jul;29(7):1320-6. doi: 10.1097/HJH.0b013e32834705e4.
RGD ID: 8657072
Pubmed: PMID:21602714   (View Abstract at PubMed)
DOI: DOI:10.1097/HJH.0b013e32834705e4   (Journal Full-text)

OBJECTIVES: The interval harboring a quantitative trait locus for blood pressure (BP), C18QTL3, contains beta-2 adrenergic receptor (Adrb2) and neural precursor cell expressed, developmentally downregulated 4-like (Nedd4l) genes. None of the other genes in the C18QTL3-residing interval is known to affect BP. The identification of C18QTL3 might uncover a brand new gene that could prosper into a novel diagnostic and/or therapeutic target for essential hypertension, if neither Adrb2 nor Nedd4l could be upheld as candidate genes. METHODS: Congenic fine resolution was combined with gene analyses. RESULTS: The gene encoding alpha-kinase 2 (Alpk2) contains a three base-pair deletion and multiple nonconserved mutations in its coding region in Dahl salt-sensitive (DSS) rats. In contrast, the gastrin-releasing peptide gene (Grp) possesses two nonconserved mutations, designated as single nucleotide polymorphisms 1 and 2 (i.e. SNP1 and SNP2), but could not be supported as a candidate gene because the C18S.L14 congenic strain displayed a homozygous DSS genotype at both SNP1 and SNP2. Furthermore, Adrb2 and Nedd4l could not account for the BP-diminishing effect of Lewis alleles in C18S.L14, as their DSS alleles bear functionally identical domains as those of Lewis, and no evidence of differential expression and splicing was evident. No significant nucleotide variations were found in 13 other genes closely linked to Alpk2. CONCLUSION: Alpk2 emerged as a strong candidate gene for C18QTL3. The present study is the first to implicate Alpk2 in the genetics of polygenic hypertension and paves the way for novel gene discovery.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SS/JrRathypertension MODELIAGP compared to congenics with Lewis allelesRGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SS.LEW-(D18Rat61-D18Rat45)/AydRatdecreased systemic arterial blood pressure  IAGP as compared to parental SS/JrRGD 
SS.LEW-(D18Chm124-D18Chm126)/AydRatdecreased systemic arterial blood pressure  IAGP as compared to parental SS/JrRGD 
SS.LEW-(D18Chm59-D18Rat1)/AydRatdecreased systemic arterial blood pressure  IAGP as compared to parental SS/JrRGD 
SS.LEW-(D18Rat55-D18Mgh2)/AydRatdecreased systemic arterial blood pressure  IAGP as compared to parental SS/JrRGD 
SS.LEW-(D18Wox7-D18Rat67)/AydRatdecreased systemic arterial blood pressure  IAGP as compared to parental SS/JrRGD 
SS/JrRatsalt-sensitive hypertension susceptibilityIAGP compared to congenics with Lewis allelesRGD 

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Objects referenced in this article
QTL Bp319 Blood pressure QTL 319 Rattus norvegicus
Strain SS.LEW-(D18Chm90-D18Chm4)/Ayd null Rattus norvegicus

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