1et1: Difference between revisions

Latest revision as of 07:06, 7 February 2024

CRYSTAL STRUCTURE OF HUMAN PARATHYROID HORMONE 1-34 AT 0.9 A RESOLUTION

Structural highlights

1et1 is a 2 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:	X-ray diffraction, Resolution 0.9Å
Ligands:	NA
Resources:	FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

PTHY_HUMAN Defects in PTH are a cause of familial isolated hypoparathyroidism (FIH) [MIM:146200; also called autosomal dominant hypoparathyroidism or autosomal dominant hypocalcemia. FIH is characterized by hypocalcemia and hyperphosphatemia due to inadequate secretion of parathyroid hormone. Symptoms are seizures, tetany and cramps. FIH exist both as autosomal dominant and recessive forms of hypoparathyroidism.^[1] ^[2] ^[3]

Function

PTHY_HUMAN PTH elevates calcium level by dissolving the salts in bone and preventing their renal excretion. Stimulates [1-14C]-2-deoxy-D-glucose (2DG) transport and glycogen synthesis in osteoblastic cells.^[4]

Evolutionary Conservation

Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.

References

↑ Arnold A, Horst SA, Gardella TJ, Baba H, Levine MA, Kronenberg HM. Mutation of the signal peptide-encoding region of the preproparathyroid hormone gene in familial isolated hypoparathyroidism. J Clin Invest. 1990 Oct;86(4):1084-7. PMID:2212001 doi:https://dx.doi.org/10.1172/JCI114811
↑ Sunthornthepvarakul T, Churesigaew S, Ngowngarmratana S. A novel mutation of the signal peptide of the preproparathyroid hormone gene associated with autosomal recessive familial isolated hypoparathyroidism. J Clin Endocrinol Metab. 1999 Oct;84(10):3792-6. PMID:10523031
↑ Datta R, Waheed A, Shah GN, Sly WS. Signal sequence mutation in autosomal dominant form of hypoparathyroidism induces apoptosis that is corrected by a chemical chaperone. Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19989-94. Epub 2007 Dec 3. PMID:18056632 doi:10.1073/pnas.0708725104
↑ Zoidis E, Ghirlanda-Keller C, Schmid C. Stimulation of glucose transport in osteoblastic cells by parathyroid hormone and insulin-like growth factor I. Mol Cell Biochem. 2011 Feb;348(1-2):33-42. doi: 10.1007/s11010-010-0634-z. Epub, 2010 Nov 13. PMID:21076856 doi:10.1007/s11010-010-0634-z

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OCA

[1] Arnold A, Horst SA, Gardella TJ, Baba H, Levine MA, Kronenberg HM. Mutation of the signal peptide-encoding region of the preproparathyroid hormone gene in familial isolated hypoparathyroidism. J Clin Invest. 1990 Oct;86(4):1084-7. PMID:2212001 doi:https://dx.doi.org/10.1172/JCI114811

[2] Sunthornthepvarakul T, Churesigaew S, Ngowngarmratana S. A novel mutation of the signal peptide of the preproparathyroid hormone gene associated with autosomal recessive familial isolated hypoparathyroidism. J Clin Endocrinol Metab. 1999 Oct;84(10):3792-6. PMID:10523031

[3] Datta R, Waheed A, Shah GN, Sly WS. Signal sequence mutation in autosomal dominant form of hypoparathyroidism induces apoptosis that is corrected by a chemical chaperone. Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19989-94. Epub 2007 Dec 3. PMID:18056632 doi:10.1073/pnas.0708725104

[4] Zoidis E, Ghirlanda-Keller C, Schmid C. Stimulation of glucose transport in osteoblastic cells by parathyroid hormone and insulin-like growth factor I. Mol Cell Biochem. 2011 Feb;348(1-2):33-42. doi: 10.1007/s11010-010-0634-z. Epub, 2010 Nov 13. PMID:21076856 doi:10.1007/s11010-010-0634-z

[1]

[2]

[3]

[4]

@@ Line 3: / Line 3: @@
 <StructureSection load='1et1' size='340' side='right'caption='[[1et1]], [[Resolution|resolution]] 0.90&Aring;' scene=''>
 == Structural highlights ==
-<table><tr><td colspan='2'>[[1et1]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1ET1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1ET1 FirstGlance]. <br>
+<table><tr><td colspan='2'>[[1et1]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1ET1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1ET1 FirstGlance]. <br>
-</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 0.9&#8491;</td></tr>
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
 <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1et1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1et1 OCA], [https://pdbe.org/1et1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1et1 RCSB], [https://www.ebi.ac.uk/pdbsum/1et1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1et1 ProSAT]</span></td></tr>
 </table>
 == Disease ==
-[[https://www.uniprot.org/uniprot/PTHY_HUMAN PTHY_HUMAN]] Defects in PTH are a cause of familial isolated hypoparathyroidism (FIH) [MIM:[https://omim.org/entry/146200 146200]]; also called autosomal dominant hypoparathyroidism or autosomal dominant hypocalcemia. FIH is characterized by hypocalcemia and hyperphosphatemia due to inadequate secretion of parathyroid hormone. Symptoms are seizures, tetany and cramps. FIH exist both as autosomal dominant and recessive forms of hypoparathyroidism.<ref>PMID:2212001</ref> <ref>PMID:10523031</ref> <ref>PMID:18056632</ref>
+[https://www.uniprot.org/uniprot/PTHY_HUMAN PTHY_HUMAN] Defects in PTH are a cause of familial isolated hypoparathyroidism (FIH) [MIM:[https://omim.org/entry/146200 146200]; also called autosomal dominant hypoparathyroidism or autosomal dominant hypocalcemia. FIH is characterized by hypocalcemia and hyperphosphatemia due to inadequate secretion of parathyroid hormone. Symptoms are seizures, tetany and cramps. FIH exist both as autosomal dominant and recessive forms of hypoparathyroidism.<ref>PMID:2212001</ref> <ref>PMID:10523031</ref> <ref>PMID:18056632</ref>
 == Function ==
-[[https://www.uniprot.org/uniprot/PTHY_HUMAN PTHY_HUMAN]] PTH elevates calcium level by dissolving the salts in bone and preventing their renal excretion. Stimulates [1-14C]-2-deoxy-D-glucose (2DG) transport and glycogen synthesis in osteoblastic cells.<ref>PMID:21076856</ref>
+[https://www.uniprot.org/uniprot/PTHY_HUMAN PTHY_HUMAN] PTH elevates calcium level by dissolving the salts in bone and preventing their renal excretion. Stimulates [1-14C]-2-deoxy-D-glucose (2DG) transport and glycogen synthesis in osteoblastic cells.<ref>PMID:21076856</ref>
 == Evolutionary Conservation ==
 [[Image:Consurf_key_small.gif|200px|right]]
@@ Line 21: / Line 22: @@
 </jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1et1 ConSurf].
 <div style="clear:both"></div>
-<div style="background-color:#fffaf0;">
-== Publication Abstract from PubMed ==
-The N-terminal fragment 1-34 of parathyroid hormone (PTH), administered intermittently, results in increased bone formation in patients with osteoporosis. PTH and a related molecule, parathyroid hormone-related peptide (PTHrP), act on cells via a common PTH/PTHrP receptor. To define more precisely the ligand-receptor interactions, we have crystallized human PTH (hPTH)-(1-34) and determined the structure to 0.9-A resolution. hPTH-(1-34) crystallizes as a slightly bent, long helical dimer. Analysis reveals that the extended helical conformation of hPTH-(1-34) is the likely bioactive conformation. We have developed molecular models for the interaction of hPTH-(1-34) and hPTHrP-(1-34) with the PTH/PTHrP receptor. A receptor binding pocket for the N terminus of hPTH-(1-34) and a hydrophobic interface with the receptor for the C terminus of hPTH-(1-34) are proposed.
-Crystal structure of human parathyroid hormone 1-34 at 0.9-A resolution.,Jin L, Briggs SL, Chandrasekhar S, Chirgadze NY, Clawson DK, Schevitz RW, Smiley DL, Tashjian AH, Zhang F J Biol Chem. 2000 Sep 1;275(35):27238-44. PMID:10837469<ref>PMID:10837469</ref>
-From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-</div>
-<div class="pdbe-citations 1et1" style="background-color:#fffaf0;"></div>
 == References ==
 <references/>
 __TOC__
 </StructureSection>
-[[Category: Human]]
+[[Category: Homo sapiens]]
 [[Category: Large Structures]]
-[[Category: Briggs, S L]]
+[[Category: Briggs SL]]
-[[Category: Chandrasekhar, S]]
+[[Category: Chandrasekhar S]]
-[[Category: Chirgadze, N Y]]
+[[Category: Chirgadze NY]]
-[[Category: Clawson, D K]]
+[[Category: Clawson DK]]
-[[Category: Jin, L]]
+[[Category: Jin L]]
-[[Category: Schevitz, R W]]
+[[Category: Schevitz RW]]
-[[Category: Smiley, D L]]
+[[Category: Smiley DL]]
-[[Category: Tashjian, A H]]
+[[Category: Tashjian AH]]
-[[Category: Zhang, F]]
+[[Category: Zhang F]]
-[[Category: Helical dimer]]
-[[Category: Hormone-growth factor complex]]

1et1: Difference between revisions

Latest revision as of 07:06, 7 February 2024

CRYSTAL STRUCTURE OF HUMAN PARATHYROID HORMONE 1-34 AT 0.9 A RESOLUTION

Structural highlights

Disease

Function

Evolutionary Conservation

References

Contents

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