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1v18

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(New page: 200px<br /> <applet load="1v18" size="450" color="white" frame="true" align="right" spinBox="true" caption="1v18, resolution 2.1&Aring;" /> '''THE CRYSTAL STRUCTUR...)
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[[Image:1v18.gif|left|200px]]<br /><applet load="1v18" size="350" color="white" frame="true" align="right" spinBox="true"
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<applet load="1v18" size="450" color="white" frame="true" align="right" spinBox="true"
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caption="1v18, resolution 2.1&Aring;" />
caption="1v18, resolution 2.1&Aring;" />
'''THE CRYSTAL STRUCTURE OF BETA-CATENIN ARMADILLO REPEAT COMPLEXED WITH A PHOSPHORYLATED APC 20MER REPEAT.'''<br />
'''THE CRYSTAL STRUCTURE OF BETA-CATENIN ARMADILLO REPEAT COMPLEXED WITH A PHOSPHORYLATED APC 20MER REPEAT.'''<br />
==Overview==
==Overview==
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The transcriptional coactivator beta-catenin mediates Wnt growth factor, signaling. In the absence of a Wnt signal, casein kinase 1 (CK1) and, glycogen synthase kinase-3beta (GSK-3beta) phosphorylate cytosolic, beta-catenin, thereby flagging it for recognition and destruction by the, ubiquitin/proteosome machinery. Phosphorylation occurs in a multiprotein, complex that includes the kinases, beta-catenin, axin, and the Adenomatous, Polyposis Coli (APC) protein. The role of APC in this process is poorly, understood. CK1epsilon and GSK-3beta phosphorylate APC, which increases, its affinity for beta-catenin. Crystal structures of phosphorylated and, nonphosphorylated APC bound to beta-catenin reveal a, phosphorylation-dependent binding motif generated by mutual priming of CK1, and GSK-3beta substrate sequences. Axin is shown to act as a scaffold for, substrate phosphorylation by these kinases. Phosphorylated APC and axin, bind to the same surface of, and compete directly for, beta-catenin. The, structural and biochemical data suggest a novel model for how APC, functions in beta-catenin degradation.
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The transcriptional coactivator beta-catenin mediates Wnt growth factor signaling. In the absence of a Wnt signal, casein kinase 1 (CK1) and glycogen synthase kinase-3beta (GSK-3beta) phosphorylate cytosolic beta-catenin, thereby flagging it for recognition and destruction by the ubiquitin/proteosome machinery. Phosphorylation occurs in a multiprotein complex that includes the kinases, beta-catenin, axin, and the Adenomatous Polyposis Coli (APC) protein. The role of APC in this process is poorly understood. CK1epsilon and GSK-3beta phosphorylate APC, which increases its affinity for beta-catenin. Crystal structures of phosphorylated and nonphosphorylated APC bound to beta-catenin reveal a phosphorylation-dependent binding motif generated by mutual priming of CK1 and GSK-3beta substrate sequences. Axin is shown to act as a scaffold for substrate phosphorylation by these kinases. Phosphorylated APC and axin bind to the same surface of, and compete directly for, beta-catenin. The structural and biochemical data suggest a novel model for how APC functions in beta-catenin degradation.
==Disease==
==Disease==
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Known diseases associated with this structure: Adenoma, periampullary OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Adenomatous polyposis coli OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Adenomatous polyposis coli, attenuated OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Colorectal cancer OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Desmoid disease, hereditary OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Gardner syndrome OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Gastric cancer OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]], Turcot syndrome OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=175100 175100]]
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Known diseases associated with this structure: Adenoma, periampullary OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Adenomatous polyposis coli OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Brain tumor-polyposis syndrome 2 OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Colorectal cancer, somatic OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Desmoid disease, hereditary OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Gardner syndrome OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Gastric cancer, somatic OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]], Hepatoblastoma OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=611731 611731]]
==About this Structure==
==About this Structure==
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1V18 is a [http://en.wikipedia.org/wiki/Protein_complex Protein complex] structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://ispc.weizmann.ac.il/oca-bin/ocashort?id=1V18 OCA].
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1V18 is a [http://en.wikipedia.org/wiki/Protein_complex Protein complex] structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1V18 OCA].
==Reference==
==Reference==
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[[Category: Mus musculus]]
[[Category: Mus musculus]]
[[Category: Protein complex]]
[[Category: Protein complex]]
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[[Category: Ha, N.C.]]
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[[Category: Ha, N C.]]
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[[Category: Weis, W.I.]]
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[[Category: Weis, W I.]]
[[Category: beta-catenin degradation complex]]
[[Category: beta-catenin degradation complex]]
[[Category: cell adhesion]]
[[Category: cell adhesion]]
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[[Category: wnt signal]]
[[Category: wnt signal]]
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''Page seeded by [http://ispc.weizmann.ac.il/oca OCA ] on Mon Nov 12 19:40:47 2007''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 15:30:31 2008''

Revision as of 13:30, 21 February 2008


1v18, resolution 2.1Å

Drag the structure with the mouse to rotate

THE CRYSTAL STRUCTURE OF BETA-CATENIN ARMADILLO REPEAT COMPLEXED WITH A PHOSPHORYLATED APC 20MER REPEAT.

Contents

Overview

The transcriptional coactivator beta-catenin mediates Wnt growth factor signaling. In the absence of a Wnt signal, casein kinase 1 (CK1) and glycogen synthase kinase-3beta (GSK-3beta) phosphorylate cytosolic beta-catenin, thereby flagging it for recognition and destruction by the ubiquitin/proteosome machinery. Phosphorylation occurs in a multiprotein complex that includes the kinases, beta-catenin, axin, and the Adenomatous Polyposis Coli (APC) protein. The role of APC in this process is poorly understood. CK1epsilon and GSK-3beta phosphorylate APC, which increases its affinity for beta-catenin. Crystal structures of phosphorylated and nonphosphorylated APC bound to beta-catenin reveal a phosphorylation-dependent binding motif generated by mutual priming of CK1 and GSK-3beta substrate sequences. Axin is shown to act as a scaffold for substrate phosphorylation by these kinases. Phosphorylated APC and axin bind to the same surface of, and compete directly for, beta-catenin. The structural and biochemical data suggest a novel model for how APC functions in beta-catenin degradation.

Disease

Known diseases associated with this structure: Adenoma, periampullary OMIM:[611731], Adenomatous polyposis coli OMIM:[611731], Brain tumor-polyposis syndrome 2 OMIM:[611731], Colorectal cancer, somatic OMIM:[611731], Desmoid disease, hereditary OMIM:[611731], Gardner syndrome OMIM:[611731], Gastric cancer, somatic OMIM:[611731], Hepatoblastoma OMIM:[611731]

About this Structure

1V18 is a Protein complex structure of sequences from Homo sapiens and Mus musculus. Full crystallographic information is available from OCA.

Reference

Mechanism of phosphorylation-dependent binding of APC to beta-catenin and its role in beta-catenin degradation., Ha NC, Tonozuka T, Stamos JL, Choi HJ, Weis WI, Mol Cell. 2004 Aug 27;15(4):511-21. PMID:15327768

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