IKK2

Inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta
Identifiers
Symbol(s)	IKBKB; FLJ40509; IKK-beta; IKK2; IKKB; MGC131801; NFKBIKB
External IDs	OMIM: 603258 MGI: 1338071 Homologene: 7782
Gene Ontology Molecular Function: • nucleotide binding • protein serine/threonine kinase activity • protein-tyrosine kinase activity • ATP binding • transcription activator activity • transferase activity • identical protein binding Cellular Component: • cytoplasm Biological Process: • B cell homeostasis • protein amino acid phosphorylation • activation of NF-kappaB transcription factor
RNA expression pattern
Additional recommended knowledge Daily Sensitivity Test What is the Correct Way to Check Repeatability in Balances? Guide to balance cleaning: 8 simple steps More reference expression data
Orthologs
	Human	Mouse
Entrez	3551	16150
Ensembl	ENSG00000104365	ENSMUSG00000031537
Uniprot	O14920	Q05DR8
Refseq	NM_001556 (mRNA) NP_001547 (protein)	NM_010546 (mRNA) NP_034676 (protein)
Location	Chr 8: 42.25 - 42.31 Mb	Chr 8: 24.12 - 24.17 Mb
Pubmed search	[1]	[2]

IKK2 is the name of a protein that plays a significant factor in the state of brain cells after a stroke. In a stroke, a communications network between cells called NF-kB (nuclear factor-kappa B) is activated by IKK2. If this signal activating NF-kB is blocked, then damaged cells within the brain stay alive, and according to a study performed by the University of Heidelberg and the University of Ulm, the cells even appear to make some recovery.^[1] The size of the infarct, or tissue killed or damaged by ischemia, is reduced in mice in which IKK2 has been blocked.^[2] Additionally, experimental mice that had an overactive form of IKK2 experienced the loss of many more neurons than controls did after a stroke-simulating event.^[1] Researchers found a molecule that could block the signalling of IKK2, and they learned that the protective effect of blocking IKK2 still took place up to four and a half hours after the insult.^[3] This fact could have important implications for treatment of human patients with stroke if blocking IKK2 is developed as a treatment, since many patients do not reach the hospital soon enough to be helped by treatments that are only effective for a short period.

In another study, researchers found that inhibiting IKK2 prevented kidney and wasting diseases in an animal model of wasting diseases often found in human AIDS sufferers.^[4]

References

1. ^ ^{a b} BBC News. 14 November 2005. Stroke 'cell-death trigger' found. Retrieved on June 28, 2007.
2. ^ Schwaninger M, Inta I, Herrmann O. 2006. NF-kappaB signalling in cerebral ischaemia. Biochemical Society Transactions. Volume 34, Pt 6, Pages 1291-1294. PMID 17073804. Retrieved on June 28, 2007.
3. ^ Herrmann O, Baumann B, de Lorenzi R, Muhammad S, Zhang W, Kleesiek J, Malfertheiner M, Köhrmann M, Potrovita I, Maegele I, Beyer C, Burke JR, Hasan MT, Bujard H, Wirth T, Pasparakis M, Schwaninger M. 2005. IKK mediates ischemia-induced neuronal death. Nature Medicine. Volume 11, Issue 12, Pages 1322-1329. PMID 16286924. Retrieved on June 28, 2007.
4. ^ Heckmann A, Waltzinger C, Jolicoeur P, Dreano M, Kosco-Vilbois MH, and Sagot Y. 2004. IKK2 Inhibitor Alleviates Kidney and Wasting Diseases in a Murine Model of Human AIDS. American Journal of Pathology. Volume 164, Pages 1253-1262. Retrieved on June 30, 2007.

See also

• IκB kinase