B6.129-Grk3^tm1Rjl/J

Stock number: 012431
Research areas: Neurobiology Research, Sensorineural Research

Description

Adrbk2 (adrenergic receptor kinase, beta 2; also called GRK3) is the major G protein-coupled receptor kinase family member in olfactory neurons, and mice lacking GRK3 exhibit a deficit in desensitization to olfactants. In homozygous mice, airway smooth muscle cells exhibit supersensitivity to muscarinic agents, and brain neurons exhibit altered kappa opioid receptor-dependent tolerance.

Detailed description

Adrbk2 (adrenergic receptor kinase, beta 2; also called GRK3) is the major G protein-coupled receptor kinase family member in olfactory neurons, and mice lacking GRK3 exhibit a deficit in desensitization to olfactants. In homozygous mice, airway smooth muscle cells exhibit supersensitivity to muscarinic agents, and brain neurons exhibit altered kappa opioid receptor-dependent tolerance. Expression is eliminated in olfactory neuroepithelium, brain, and airway smooth muscle cells.

Development

Exons 7 and 8 (encoding part of the protein kinase catalytic domain) were replaced with a PGK-neomycin resistance cassette (in the antisense orientation). The mutation was created in a 129-derived embryonic stem (ES) cell line. The strain was backcrossed more than ten times to C57BL/6 by the donating laboratory.

Allele

Symbol: Grk3^tm1Rjl
Name: targeted mutation 1, Robert J Lefkowitz
MGI accession ID: MGI:2429934
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: GRK3 (-)
Marker symbol: Grk3
Marker name: G protein-coupled receptor kinase 3
Marker synonyms: 4833444A01Rik; Adrbk2; Adrbk-2; BARK2; Bark-2; beta ARK2
Chromosome: 5
Strain of origin: 129
Molecular note: Exons 7 and 8 (encoding part of the protein kinase catalytic domain) were replaced with a PGK-neomycin resistance cassette (in the antisense orientation) by homologous recombination. Included in the deleted region was sequence encoding the ATP binding motif of catalytic subdomain I. While transcript was detected by Northern blot analysis of homozygous mutant mice, the absence of protein was verified by Western blot analysis.