NLRP4 and CHUK

Number of citations of the paper that reports this interaction (PubMedID 12093792)
40

Data Source:
HPRD (in vivo, in vitro)

		NLRP4	CHUK
Description		NLR family pyrin domain containing 4	component of inhibitor of nuclear factor kappa B kinase complex
Image
GO Annotations	Cellular Component	Cytosol	Nucleoplasm Cytoplasm Cytosol IkappaB Kinase Complex Cytoplasmic Side Of Plasma Membrane CD40 Receptor Complex
	Molecular Function	ATP Binding	Protein Kinase Activity Protein Serine/threonine Kinase Activity Protein Binding ATP Binding IkappaB Kinase Activity Protein Homodimerization Activity Protein-containing Complex Binding Protein Heterodimerization Activity Scaffold Protein Binding Transferrin Receptor Binding
	Biological Process	Inflammatory Response	Skeletal Muscle Contraction Protein Phosphorylation Inflammatory Response Immune Response I-kappaB Kinase/NF-kappaB Signaling I-kappaB Phosphorylation Rho Protein Signal Transduction Response To Xenobiotic Stimulus Response To Virus Response To Toxic Substance Anatomical Structure Morphogenesis Response To Acetate Peptidyl-serine Phosphorylation Negative Regulation Of NF-kappaB Transcription Factor Activity Response To Lipopolysaccharide Positive Regulation Of Interferon-alpha Production Response To Hydroperoxide Tumor Necrosis Factor-mediated Signaling Pathway Cellular Response To Reactive Oxygen Species NIK/NF-kappaB Signaling Positive Regulation Of I-kappaB Kinase/NF-kappaB Signaling Response To Amino Acid Innate Immune Response Positive Regulation Of Transcription, DNA-templated Positive Regulation Of Transcription By RNA Polymerase II Positive Regulation Of NF-kappaB Transcription Factor Activity Striated Muscle Cell Differentiation Response To Cholecystokinin Cellular Response To Cadmium Ion Cellular Response To Tumor Necrosis Factor Cellular Response To Virus
Pathways		IRF3 mediated activation of type 1 IFN Regulation of innate immune responses to cytosolic DNA IRF3-mediated induction of type I IFN	Activation of NF-kappaB in B cells Activation of NF-kappaB in B cells ER-Phagosome pathway NOD1/2 Signaling Pathway TICAM1, RIP1-mediated IKK complex recruitment RIP-mediated NFkB activation via ZBP1 AKT phosphorylates targets in the cytosol Downstream TCR signaling FCERI mediated NF-kB activation TAK1 activates NFkB by phosphorylation and activation of IKKs complex Regulation of TNFR1 signaling TNFR1-induced NFkappaB signaling pathway IKBKB deficiency causes SCID IKBKG deficiency causes anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID) (via TLR) IkBA variant leads to EDA-ID Dectin-1 mediated noncanonical NF-kB signaling CLEC7A (Dectin-1) signaling Constitutive Signaling by AKT1 E17K in Cancer NIK-->noncanonical NF-kB signaling MAP3K8 (TPL2)-dependent MAPK1/3 activation Interleukin-1 signaling TRAF6 mediated NF-kB activation NF-kB activation through FADD/RIP-1 pathway mediated by caspase-8 and -10 IRAK1 recruits IKK complex IKK complex recruitment mediated by RIP1 IRAK1 recruits IKK complex upon TLR7/8 or 9 stimulation
Drugs			Aminosalicylic acid Mesalazine Sulfasalazine Acetylcysteine
Diseases
GWAS		Plasma anti-thyroglobulin levels ( 29678681)	Liver enzyme levels ( 18940312) Psoriasis ( 28537254) Psoriasis or type 2 diabetes (trans-disease meta-analysis) ( 33385400) Type 2 diabetes ( 30054458)
Interacting Genes		2 interacting genes: CHUK NLRC4	80 interacting genes: AKT1 AKT2 AMBRA1 ATR BCL10 BCL3 BTRC CASP8 CDC37 CHEK1 CREBBP CSF2RA CSNK2A1 CTNNB1 CUEDC2 CUL1 DCUN1D5 E2F4 EIF2AK2 ELP1 ERBIN ESR1 FKBP5 FOXO3 H3-4 H3C14 HSP90AA1 HSP90AB1 HTT IFIT5 IKBKB IKBKE IKBKG IRS1 MAP3K1 MAP3K11 MAP3K14 MAP3K4 MAP3K7 MAP3K8 NCOA3 NCOR1 NCOR2 NFKB1 NFKB2 NFKBIA NFKBIB NLRP4 NOTCH3 NR2C2 PAX8 PEBP1 PIAS1 PRKCB PRKCI PRKCQ PRKDC PTPN11 RELA RICTOR RIPK2 RPL27 SRC SRPK1 SRPK2 STAP2 TANK TGFBR1 TNFAIP3 TNFRSF1A TP53 TRAF2 TRAF3IP2 TRAF4 TRIM27 TRPC4AP UBC UBE2E3 UBE2I UBE2N
Entrez ID		147945	1147
HPRD ID		09619	02811
Ensembl ID		ENSG00000160505	ENSG00000213341
Uniprot IDs		B2RCA1 Q96MN2	O15111
PDB IDs		4EWI	3BRT 5EBZ 5TQW 5TQX 5TQY
Enriched GO Terms of Interacting Partners?
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