1t29
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[1t29]] 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=1T29 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1T29 FirstGlance]. <br> | <table><tr><td colspan='2'>[[1t29]] 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=1T29 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1T29 FirstGlance]. <br> | ||
| - | </td></tr><tr><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr> | + | </td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></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=1t29 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1t29 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1t29 RCSB], [http://www.ebi.ac.uk/pdbsum/1t29 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=1t29 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1t29 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1t29 RCSB], [http://www.ebi.ac.uk/pdbsum/1t29 PDBsum]</span></td></tr> |
| - | <table> | + | </table> |
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue. [[http://www.uniprot.org/uniprot/FANCJ_HUMAN FANCJ_HUMAN]] Defects in BRIP1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.<ref>PMID:11301010</ref> <ref>PMID:14983014</ref> <ref>PMID:16153896</ref> <ref>PMID:16116421</ref> Defects in BRIP1 are the cause of Fanconi anemia complementation group J (FANCJ) [MIM:[http://omim.org/entry/609054 609054]]. It is a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.<ref>PMID:16153896</ref> <ref>PMID:16116421</ref> <ref>PMID:20639400</ref> <ref>PMID:16116424</ref> <ref>PMID:16116423</ref> | [[http://www.uniprot.org/uniprot/BRCA1_HUMAN BRCA1_HUMAN]] Defects in BRCA1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Note=Mutations in BRCA1 are thought to be responsible for 45% of inherited breast cancer. Moreover, BRCA1 carriers have a 4-fold increased risk of colon cancer, whereas male carriers face a 3-fold increased risk of prostate cancer. Cells lacking BRCA1 show defects in DNA repair by homologous recombination.<ref>PMID:11301010</ref> <ref>PMID:15133502</ref> <ref>PMID:7545954</ref> <ref>PMID:12427738</ref> <ref>PMID:18285836</ref> <ref>PMID:7939630</ref> <ref>PMID:7894491</ref> <ref>PMID:7894493</ref> <ref>PMID:8554067</ref> <ref>PMID:8776600</ref> <ref>PMID:8723683</ref> <ref>PMID:9760198</ref> <ref>PMID:9482581</ref> <ref>PMID:9609997</ref> <ref>PMID:10323242</ref> <ref>PMID:12442275</ref> <ref>PMID:12938098</ref> <ref>PMID:14722926</ref> Defects in BRCA1 are a cause of susceptibility to familial breast-ovarian cancer type 1 (BROVCA1) [MIM:[http://omim.org/entry/604370 604370]]. A condition associated with familial predisposition to cancer of the breast and ovaries. Characteristic features in affected families are an early age of onset of breast cancer (often before age 50), increased chance of bilateral cancers (cancer that develop in both breasts, or both ovaries, independently), frequent occurrence of breast cancer among men, increased incidence of tumors of other specific organs, such as the prostate. Note=Mutations in BRCA1 are thought to be responsible for more than 80% of inherited breast-ovarian cancer. Defects in BRCA1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[http://omim.org/entry/167000 167000]]. The term ovarian cancer defines malignancies originating from ovarian tissue. Although many histologic types of ovarian tumors have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in BRCA1 are a cause of susceptibility to pancreatic cancer type 4 (PNCA4) [MIM:[http://omim.org/entry/614320 614320]]. A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue. [[http://www.uniprot.org/uniprot/FANCJ_HUMAN FANCJ_HUMAN]] Defects in BRIP1 are a cause of susceptibility to breast cancer (BC) [MIM:[http://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.<ref>PMID:11301010</ref> <ref>PMID:14983014</ref> <ref>PMID:16153896</ref> <ref>PMID:16116421</ref> Defects in BRIP1 are the cause of Fanconi anemia complementation group J (FANCJ) [MIM:[http://omim.org/entry/609054 609054]]. It is a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.<ref>PMID:16153896</ref> <ref>PMID:16116421</ref> <ref>PMID:20639400</ref> <ref>PMID:16116424</ref> <ref>PMID:16116423</ref> | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Gu, L | + | [[Category: Gu, L]] |
| - | [[Category: Shi, Y | + | [[Category: Shi, Y]] |
| - | [[Category: Shiozaki, E N | + | [[Category: Shiozaki, E N]] |
| - | [[Category: Yan, N | + | [[Category: Yan, N]] |
[[Category: Bach1]] | [[Category: Bach1]] | ||
[[Category: Brca1]] | [[Category: Brca1]] | ||
Revision as of 06:52, 6 January 2015
Crystal structure of the BRCA1 BRCT repeats bound to a phosphorylated BACH1 peptide
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