Sandbox Reserved 827: Difference between revisions
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==Dimer== | ==Dimer== | ||
ULD and KD also contribute to dimerization thanks to several interactions with the SDD of the opposite subunit in the homodimer. | |||
There are several hydrogen bonds between the KD (N- and C-lobes) and the SDD of the opposite subunit: a salt bridge is formed between Asp33 in the N-lobe and Lys589 in the SDD and the strands the β7-β8 in the C-love interact with the SDD. A | There are several hydrogen bonds between the KD (N- and C-lobes) and the SDD of the opposite subunit: a | ||
<scene name='56/568025/33-589/2'>salt bridge</scene> is formed between Asp33 in the N-lobe and Lys589 in the SDD and the strands the β7-β8 in the C-love interact with the SDD. A “ | |||
<scene name='56/568025/Egr-seq/1'>EGR</scene>” sequence (residues 355–357) in the ULD interacts with the SDD: Glu355-ULD interacts with Arg444-SDD (salt bridge) and Trp445-SDD (hydrogen bonds). | |||
=Possible residue modifications= | =Possible residue modifications= | ||
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== Inflammatory response == | == Inflammatory response == | ||
The inflammatory response begin with the formation of the complex TBK1-TANK-TRAF. That allows phosphorylation of IRF3, IRF7 and DDX3X. Then these phosphorylated proteins form homodimers and they are translocated into the nucleus, where they activate transcription of interferon regulatory factors (IFN). | The inflammatory response begin with the formation of the complex TBK1-TANK-TRAF. That allows phosphorylation of IRF3, IRF7 and DDX3X. Then these phosphorylated proteins form homodimers and they are translocated into the nucleus, where they activate transcription of interferon regulatory factors (IFN). Interferons are proteins synthetized in response to recognition of pathogen. They can interact with viral replication and inhibit it. | ||
== Anti-apoptosis == | == Anti-apoptosis == | ||
The complex TBK1-TANK-TRAF phosphorylates an inhibitor of NFkappaB, which finally activates NFkappaB, an anti-apoptotic transcription factor. | The complex TBK1-TANK-TRAF phosphorylates an inhibitor of NFkappaB, which inactivates it. This finally activates NFkappaB, an anti-apoptotic transcription factor. | ||
= Diseases = | = Diseases = | ||
