GLUL antibody (clone 2B12), anti-human
€435.00
In stock
SKU
AC-AT4666a
Catalog Number: AC-AT4666a
Size: 200 µL
Isotype: mouse IgG2a Kappa
Applications: WB, E
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Size: 200 µL
Isotype: mouse IgG2a Kappa
Applications: WB, E
Request Information AC-AT4666a">Request Information
Background:
Glutamine is a main source of energy and is involved in cell proliferation, inhibition of apoptosis, and cell signaling (Haberle et al., 2005 [PubMed 16267323]). Fetal glutamine requirements are very high and depend largely on active glutamine synthesis and the release of glutamine into the fetal circulation by the placenta. Glutamine synthetase (EC 6.3.1.2), also called glutamate-ammonia ligase (GLUL), is expressed throughout the body and plays an important role in controlling body pH and in removing ammonia from the circulation. The enzyme clears L-glutamate, the major neurotransmitter in the central nervous system, from neuronal synapses (see references in Clancy et al., 1996 [PubMed 8975719]).[supplied by OMIM
Other Names:
GLNS,GS,PIG43,PIG59
Gene Name: GLUL {ECO:0000303|PubMed:30158707, ECO:0000312|HGNC:HGNC:4341}
Gene ID: 2752
Primary Accession: P15104
Other Accession:
Format:
Glutamine is a main source of energy and is involved in cell proliferation, inhibition of apoptosis, and cell signaling (Haberle et al., 2005 [PubMed 16267323]). Fetal glutamine requirements are very high and depend largely on active glutamine synthesis and the release of glutamine into the fetal circulation by the placenta. Glutamine synthetase (EC 6.3.1.2), also called glutamate-ammonia ligase (GLUL), is expressed throughout the body and plays an important role in controlling body pH and in removing ammonia from the circulation. The enzyme clears L-glutamate, the major neurotransmitter in the central nervous system, from neuronal synapses (see references in Clancy et al., 1996 [PubMed 8975719]).[supplied by OMIM
Other Names:
GLNS,GS,PIG43,PIG59
Gene Name: GLUL {ECO:0000303|PubMed:30158707, ECO:0000312|HGNC:HGNC:4341}
Gene ID: 2752
Primary Accession: P15104
Other Accession:
Format:
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