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plays a role in the biosynthesis of gamma-aminobutyric acid.
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Negative developmental regulation of GAD can be overridden by drugs known to elevate intracellular free [Ca2 (Montrer CA2 Anticorps)+]
Sodium salicylate can regulate differently ABR threshold and expression of glutamic acid decarboxylase in spiral ganglion of juvenile and adult guinea pigs.
Our results demonstrate that GAD67 plays an important role in Alzheimer's disease pathology
Results suggest age-dependent decrease of GAD65 (Montrer GAD2 Anticorps)/67 mRNAs but normal densities of certain GABAergic interneurons in the Shank3 (Montrer SHANK3 Anticorps) transgenic mice.
GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox (Montrer PRRX1 Anticorps) genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert glutamate (Montrer GRIN1 Anticorps) to GABA.
These findings reveal that Th and Gad1 share a transcription regulatory mechanism that facilitates odorant-dependent regulation of dopamine and GABA expression levels.
Study describes in detail a population of choline acetyltransferase immunoreactive /glutamate decarboxylase 67 neurons predominantly ventral to the central canal of the cervical, thoracic and lumbar spinal cord of adult and juvenile mice. These cells potentially correspond to a sub-population of the cholinergic central canal cluster cells which may play a unique role in controlling spinal cord circuitry.
This study demonstrated that Alterations in hypoglossal motor neurons due to GAD67 deficiency in mice.
Treadmill running prevented partial sciatic nerve ligation-induced reductions in GAD65 (Montrer GAD2 Anticorps)/67 production, and, thus, GABA levels may be retained in interneurons and neuropils in the superficial dorsal horn.
Gad1 knockdown mice have pronounced sensorimotor gating deficits, increased novelty-seeking and reduced fear extinction
Glutamate decarboxylase (Montrer GLUL Anticorps) expression may be a reliable proxy of altered GABAergic transmission.
Activity deprivation due to TTX preferentially down-regulated GAD67. BDNF (Montrer BDNF Anticorps)-induced increase in the GAD67 protein was markedly lower than that of GAD65 (Montrer GAD2 Anticorps), indicating that BDNF (Montrer BDNF Anticorps) differentially regulates activity-dependent gene expression of the 2 isoforms.
plays a role in the biosynthesis of gamma-aminobutyric acid
, glutamic acid decarboxylase
, glutamic acid decarboxylase 1
, glutamic acid decarboxylase-1
, vesicular glutamic acid decarboxylase
, glutamate decarboxylase 1
, 67 kDa glutamic acid decarboxylase
, Glutamate decarboxylase 1 (brain)
, glutamate decarboxylase 1 variant GAD67NT
, glutamate decarboxylase 67 kDa isoform
, GLUTAMATE DECARBOXYLASE, 67 KD ISOFORM (GAD-67) (67 KD GLUTAMIC ACID DECARBOXYLASE)