Sandbox Reserved 827: Difference between revisions
Léa Faivre (talk | contribs) No edit summary |
Léa Faivre (talk | contribs) No edit summary |
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<Structure load='4IM3' size='400' frame='true' align='right' caption='TBK1' scene='Insert optional scene name here' /> | <Structure load='4IM3' size='400' frame='true' align='right' caption='TBK1' scene='Insert optional scene name here' /> | ||
= Global structure = | |||
=Protomer= | ==Protomer== | ||
'''Kinase domain :''' | '''Kinase domain :''' | ||
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'''Coiled coil :''' | '''Coiled coil :''' | ||
=Dimer= | ==Dimer== | ||
= Possible residue modifications = | |||
Several residues of TBK1 can be modified, by phosphorylation or polyubiquitination. | Several residues of TBK1 can be modified, by phosphorylation or polyubiquitination. | ||
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= Diseases = | |||
'''Interaction with viral proteins :''' | '''Interaction with viral proteins :''' | ||
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In case of some cancers, the permanent activation of TBK1 may be responsible of the proliferation of the cancerous cells. Since the substrates of TBK1 are involved in the proliferation pathway when phosphorylated, this permanent activation is a reason of the non apoptosis state of cells, and therefore of their proliferation. | In case of some cancers, the permanent activation of TBK1 may be responsible of the proliferation of the cancerous cells. Since the substrates of TBK1 are involved in the proliferation pathway when phosphorylated, this permanent activation is a reason of the non apoptosis state of cells, and therefore of their proliferation. | ||
= References = | |||
Q05127 | Q05127 |