1djl
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[1djl]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1DJL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1DJL FirstGlance]. <br> | <table><tr><td colspan='2'>[[1djl]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1DJL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1DJL FirstGlance]. <br> | ||
| - | </td></tr><tr><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NAP:NADP+NICOTINAMIDE-ADENINE-DINUCLEOTIDE+PHOSPHATE'>NAP</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>< | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NAP:NADP+NICOTINAMIDE-ADENINE-DINUCLEOTIDE+PHOSPHATE'>NAP</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> |
| - | <tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/NAD(P)(+)_transhydrogenase_(B-specific) NAD(P)(+) transhydrogenase (B-specific)], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=1.6.1.1 1.6.1.1] </span></td></tr> | + | <tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/NAD(P)(+)_transhydrogenase_(B-specific) NAD(P)(+) transhydrogenase (B-specific)], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=1.6.1.1 1.6.1.1] </span></td></tr> |
| - | <tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1djl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1djl OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1djl RCSB], [http://www.ebi.ac.uk/pdbsum/1djl PDBsum]</span></td></tr> | + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1djl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1djl OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1djl RCSB], [http://www.ebi.ac.uk/pdbsum/1djl PDBsum]</span></td></tr> |
| - | <table> | + | </table> |
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/NNTM_HUMAN NNTM_HUMAN]] Defects in NNT are the cause of glucocorticoid deficiency type 4 (GCCD4) [MIM:[http://omim.org/entry/614736 614736]]. A rare, potentially lethal, autosomal recessive disorder characterized by resistance to ACTH action on the adrenal cortex, adrenal insufficiency and an inability of the adrenal cortex to produce cortisol. It usually presents in the neonatal period or in early childhood with episodes of hypoglycemia and other symptoms related to cortisol deficiency, including failure to thrive, recurrent illnesses or infections, convulsions, and shock. In a small number of patients hypoglycemia can be sufficiently severe and persistent that it leads to serious long-term neurological damage or death. The diagnosis is readily confirmed with a low plasma cortisol measurement in the presence of an elevated ACTH level, and normal aldosterone and plasma renin measurements.<ref>PMID:22634753</ref> | [[http://www.uniprot.org/uniprot/NNTM_HUMAN NNTM_HUMAN]] Defects in NNT are the cause of glucocorticoid deficiency type 4 (GCCD4) [MIM:[http://omim.org/entry/614736 614736]]. A rare, potentially lethal, autosomal recessive disorder characterized by resistance to ACTH action on the adrenal cortex, adrenal insufficiency and an inability of the adrenal cortex to produce cortisol. It usually presents in the neonatal period or in early childhood with episodes of hypoglycemia and other symptoms related to cortisol deficiency, including failure to thrive, recurrent illnesses or infections, convulsions, and shock. In a small number of patients hypoglycemia can be sufficiently severe and persistent that it leads to serious long-term neurological damage or death. The diagnosis is readily confirmed with a low plasma cortisol measurement in the presence of an elevated ACTH level, and normal aldosterone and plasma renin measurements.<ref>PMID:22634753</ref> | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Cotton, N P | + | [[Category: Cotton, N P]] |
| - | [[Category: Jackson, J B | + | [[Category: Jackson, J B]] |
| - | [[Category: Peak, S J | + | [[Category: Peak, S J]] |
| - | [[Category: White, S A | + | [[Category: White, S A]] |
[[Category: Oxidoreductase]] | [[Category: Oxidoreductase]] | ||
[[Category: Rossmann fold dinucleotide binding fold reverse binding of nadp]] | [[Category: Rossmann fold dinucleotide binding fold reverse binding of nadp]] | ||
Revision as of 20:50, 22 December 2014
THE CRYSTAL STRUCTURE OF HUMAN TRANSHYDROGENASE DOMAIN III WITH BOUND NADP
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