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Search Thermo Fisher Scientific
Sequence of this protein is as follows: MASSTPSSSA TSSNAGADPN TTNLRPTTYD TWCGVAHGCT RKLGLKICGF LQRTNSLEEK SRLVSAFKER QSSKNLLSCE NSDRDARFRR TETDFSNLFA RDLLPAKNGE EQTVQFLLEV VDILLNYVRK TFDRSTKVLD FHHPHQLLEG MEGFNLELSD HPESLEQILV DCRDTLKYGV RTGHPRFFNQ LSTGLDIIGL AGEWLTSTAN TNMFTYEIAP VFVLMEQITL KKMREIVGWS SKDGDGIFSP GGAISNMYSI MAARYKYFPE VKTKGMAAVP KLVLFTSEQS RYSIKKAGAA LGFGTDNVIL IKCNERGEII PADFEAKILE AKQKGYVPFY VNATAGTTVY GAFDPIQEIA DICEKYNLWL HVDAAWGGGL LMSRKHRHKL NGIERANSVT WNPHKMMGVL LQCSAILVKE KGILQGCNQM CAGYLFQPDK QYDVSYDTGD KAIQCGRHVD IFKFWLMWKA KGTVGFENQI NKCLELAEYL YAKIKNREEF EMVFNGEPEH TNVCFWYIPQ SLRGVPDSPQ RREKLHKVAP KIKALMMESG TTMVGYQPQG DKANFFRMVI SNPAATQSDI DFLIEEIERL GQDL
GAD-65 and GAD-67 are members of the group II decarboxylase family of proteins and are responsible for catalyzing the rate limiting step in the production of GABA (gamma-aminobutyric acid) from L-glutamic acid. Although both GADs are found in the brain, GAD-65 localizes to synaptic vesicle membranes in nerve terminals, while GAD-67 is distributed throughout the cell. GAD-67 is responsible for the basal levels of GABA synthesis. In the case of a heightened demand for GABA in neurotransmission, GAD-65 will transiently activate to assist in GABA production. The loss of GAD-65 is detrimental and can impair GABA neurotransmission, however the loss of GAD-67 is lethal. Due to alternative splicing, two isoforms exist for GAD-67: the predominant GAD-67 form and the minor GAD-25 form.
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Protein Aliases: 67 kDa glutamic acid decarboxylase; FLJ45882; GAD 67; GAD-67; Glutamate decarboxylase 1; glutamate decarboxylase 1 (brain, 67kDa); Glutamate decarboxylase 67 kDa isoform; OTTHUMP00000041055
Gene Aliases: CPSQ1; GAD; GAD1; GAD67; SCP
UniProt ID: (Human) Q99259
Entrez Gene ID: (Human) 2571
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