Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.23 (
beta-galactosidase
)
14,648
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The
neural recognition molecule NB-3
, which belongs to the contactin subgroup of the immunoglobulin superfamily, is expressed exclusively in the nervous system and mainly upregulated at the early postnatal stage during mouse brain development. The expression of
NB-3
in the cerebellum increases until adulthood. In contrast, the expression in the cerebrum declines to a low level after postnatal day 7. To characterize the functional roles of
NB-3
in vivo, we generated
NB-3
-deficient mice by substituting a part of the
NB-3
gene with the
beta-galactosidase
(Lac Z) gene. Complete overlap of the Lac Z expression in the heterozygous mouse brain with the
NB-3
immunostaining pattern in the rat cerebellum and with the previously reported pattern of in situ hybridization of
NB-3
transcripts indicated that Lac Z expression reflects the expression of
NB-3
in the mouse brain.
NB-3
-deficient mice were viable and fertile. The formation and organization of all nuclei and layers throughout the brains of mutant mice appeared normal. Behavioral tests to examine motor function showed that the mice deficient for
NB-3
were slow to learn to stay on the rotating rod in the rotorod test during repeated trials, and that they displayed dysfunction of equilibrium and vestibular senses in the wire hang and horizontal rod-walking tests. In contrast, the mutant mice showed no difference of grasp force from the wild-type mice. Thus,
NB-3
-deficient mice are impaired in motor coordination.
...
PMID:Impaired motor coordination in mice lacking neural recognition molecule NB-3 of the contactin/F3 subgroup. 1288 64
