gad 67造句

• GAD 67 and GAD 65 are also regulated differently post-translationally.
• The mechanism underlying the decreased levels of GAD 67 in schizophrenic patients remains unclear.
• GAD 67 is spread evenly throughout the cell while GAD 65 is localized to nerve terminals.
• These isoforms are GAD 67 and GAD 65 with molecular weights of 67 and 65 kDa, respectively.
• GAD 67 is transcribed during early development, while GAD 65 is not transcribed until later in life.
• Both GAD 67 and GAD 65 are targets of autoantibodies in people who later develop type 1 diabetes mellitus or latent autoimmune diabetes.
• GAD 65 and GAD 67 synthesize GABA at different locations in the cell, at different developmental times, and for functionally different purposes.
• The most pronounced downregulation of GAD 67 was found in hippocampal stratum oriens layer in both disorders and in other layers and structures of hippocampus with varying degrees.
• Both GAD 65 and GAD 67 are regulated via phosphorylation, but the regulation of these isoforms differs; GAD 65 is activated by phosphorylation while GAD 67 is inhibited by phosphorylation.
• Both GAD 65 and GAD 67 are regulated via phosphorylation, but the regulation of these isoforms differs; GAD 65 is activated by phosphorylation while GAD 67 is inhibited by phosphorylation.
• GAD 67 is phosphorylated at threonine 91 by protein kinase A ( PKA ), while GAD 65 is phosphorylated, and therefore regulated by, protein kinase C ( PKC ).
• GAD 67 is a key enzyme involved in the synthesis of inhibitory neurotransmitter GABA and schizophrenic patients have been shown to express lower amounts of GAD 67 in the dorsolateral prefrontal cortex compared to healthy controls.
• GAD 67 is a key enzyme involved in the synthesis of inhibitory neurotransmitter GABA and schizophrenic patients have been shown to express lower amounts of GAD 67 in the dorsolateral prefrontal cortex compared to healthy controls.
• Some have proposed that an immediate early gene, Zif268, which normally binds to the promoter region of GAD 67 and increases transcription of GAD 67, is lower in schizophrenic patients, thus contributing to decreased levels of GAD 67.
• Some have proposed that an immediate early gene, Zif268, which normally binds to the promoter region of GAD 67 and increases transcription of GAD 67, is lower in schizophrenic patients, thus contributing to decreased levels of GAD 67.
• Some have proposed that an immediate early gene, Zif268, which normally binds to the promoter region of GAD 67 and increases transcription of GAD 67, is lower in schizophrenic patients, thus contributing to decreased levels of GAD 67.
• This developmental difference in GAD 67 and GAD 65 reflects the functional properties of each isoform; GAD 67 is needed throughout development for normal cellular functioning, while GAD 65 is not needed until slightly later in development when synaptic inhibition is more prevalent.
• This developmental difference in GAD 67 and GAD 65 reflects the functional properties of each isoform; GAD 67 is needed throughout development for normal cellular functioning, while GAD 65 is not needed until slightly later in development when synaptic inhibition is more prevalent.
• Since the dorsolateral prefrontal cortex ( DLPFC ) is involved in working memory, and GAD 67 and Zif268 mRNA levels are lower in the DLPFC of schizophrenic patients, this molecular alteration may account, at least in part, for the working memory impairments associated with the disease.
• This reflects the functional properties of the two isoforms; GAD 67 must be active at all times for normal cellular functioning, and is therefore constantly activated by PLP, while GAD 65 must only be activated when GABA neurotransmission occurs, and is therefore regulated according to the synaptic environment.