9qib: Difference between revisions

Latest revision as of 09:27, 30 September 2026

Crystal Structure of human PMS1 N-terminal domain with ATPgammaS

Structural highlights

9qib 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 2.18Å
Ligands:	AGS, MG, SO4
Resources:	FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

PMS1_HUMAN Defects in PMS1 are the cause of hereditary non-polyposis colorectal cancer type 3 (HNPCC3) [MIM:600258. Mutations in more than one gene locus can be involved alone or in combination in the production of the HNPCC phenotype (also called Lynch syndrome). Most families with clinically recognized HNPCC have mutations in either MLH1 or MSH2 genes. HNPCC is an autosomal, dominantly inherited disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early onset colorectal carcinoma (CRC) and extra-colonic cancers of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world, and accounts for 15% of all colon cancers. Cancers in HNPCC originate within benign neoplastic polyps termed adenomas. Clinically, HNPCC is often divided into two subgroups. Type I: hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II: patients have an increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected.^[1]

Function

PMS1_HUMAN Probably involved in the repair of mismatches in DNA.^[2]

References

↑ Wang Q, Lasset C, Desseigne F, Saurin JC, Maugard C, Navarro C, Ruano E, Descos L, Trillet-Lenoir V, Bosset JF, Puisieux A. Prevalence of germline mutations of hMLH1, hMSH2, hPMS1, hPMS2, and hMSH6 genes in 75 French kindreds with nonpolyposis colorectal cancer. Hum Genet. 1999 Jul-Aug;105(1-2):79-85. PMID:10480359
↑ Leung WK, Kim JJ, Wu L, Sepulveda JL, Sepulveda AR. Identification of a second MutL DNA mismatch repair complex (hPMS1 and hMLH1) in human epithelial cells. J Biol Chem. 2000 May 26;275(21):15728-32. PMID:10748105 doi:10.1074/jbc.M908768199

Proteopedia Page Contributors and Editors (what is this?)

OCA

[1] Wang Q, Lasset C, Desseigne F, Saurin JC, Maugard C, Navarro C, Ruano E, Descos L, Trillet-Lenoir V, Bosset JF, Puisieux A. Prevalence of germline mutations of hMLH1, hMSH2, hPMS1, hPMS2, and hMSH6 genes in 75 French kindreds with nonpolyposis colorectal cancer. Hum Genet. 1999 Jul-Aug;105(1-2):79-85. PMID:10480359

[2] Leung WK, Kim JJ, Wu L, Sepulveda JL, Sepulveda AR. Identification of a second MutL DNA mismatch repair complex (hPMS1 and hMLH1) in human epithelial cells. J Biol Chem. 2000 May 26;275(21):15728-32. PMID:10748105 doi:10.1074/jbc.M908768199

[1]

[2]

@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
-The entry 9qib is ON HOLD  until Paper Publication
+==Crystal Structure of human PMS1 N-terminal domain with ATPgammaS==
+<StructureSection load='9qib' size='340' side='right'caption='[[9qib]], [[Resolution|resolution]] 2.18&Aring;' scene=''>
-Authors: Bandera, A.M., Thomsen, M.
+== Structural highlights ==
+<table><tr><td colspan='2'>[[9qib]] 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=9QIB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9QIB FirstGlance]. <br>
-Description: Crystal Structure of human PMS1 N-terminal domain with ATPgammaS
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.18&#8491;</td></tr>
-[[Category: Unreleased Structures]]
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=AGS:PHOSPHOTHIOPHOSPHORIC+ACID-ADENYLATE+ESTER'>AGS</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-[[Category: Bandera, A.M]]
+<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=9qib FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9qib OCA], [https://pdbe.org/9qib PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9qib RCSB], [https://www.ebi.ac.uk/pdbsum/9qib PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9qib ProSAT]</span></td></tr>
-[[Category: Thomsen, M]]
+</table>
+== Disease ==
+[https://www.uniprot.org/uniprot/PMS1_HUMAN PMS1_HUMAN] Defects in PMS1 are the cause of hereditary non-polyposis colorectal cancer type 3 (HNPCC3) [MIM:[https://omim.org/entry/600258 600258]. Mutations in more than one gene locus can be involved alone or in combination in the production of the HNPCC phenotype (also called Lynch syndrome). Most families with clinically recognized HNPCC have mutations in either MLH1 or MSH2 genes. HNPCC is an autosomal, dominantly inherited disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early onset colorectal carcinoma (CRC) and extra-colonic cancers of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world, and accounts for 15% of all colon cancers. Cancers in HNPCC originate within benign neoplastic polyps termed adenomas. Clinically, HNPCC is often divided into two subgroups. Type I: hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II: patients have an increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected.<ref>PMID:10480359</ref>
+== Function ==
+[https://www.uniprot.org/uniprot/PMS1_HUMAN PMS1_HUMAN] Probably involved in the repair of mismatches in DNA.<ref>PMID:10748105</ref>
+== References ==
+<references/>
+__TOC__
+</StructureSection>
+[[Category: Homo sapiens]]
+[[Category: Large Structures]]
+[[Category: Bandera AM]]
+[[Category: Thomsen M]]

9qib: Difference between revisions

Latest revision as of 09:27, 30 September 2026

Crystal Structure of human PMS1 N-terminal domain with ATPgammaS

Structural highlights

Disease

Function

References

Contents

Proteopedia Page Contributors and Editors (what is this?)

Navigation menu

Page actions

Page actions

Personal tools

Navigation

Search

Tools