View source for NF-ϰB

NF-ϰB (full name is nuclear factor kappa-light-chain-enhancer of activated B Cells)&nbsp;is a protein complex that activates transcription of [[DNA|DNA]] in cells.<ref>Gilmore TD. October 2006. "Introduction to NF-kappaB: players, pathways, perspectives". Oncogene; 25(51):6680–4.</ref> It was first discovered by Dr Ranjan Sen, which was in the lab of the nobel laureate David Baltimore, using [[Electrophoretic mobility shift assay|electrophoretic mobility shift assay]] where the protein binded to a kappa enhancer sequence within [[B-cells|B cell]].&nbsp;The NK-kb transcription factors are highly conserved as they are found in organisms from the fruit fly to humans, although are absent in [[Yeast|yeast]].&nbsp;<ref>Sen R, Baltimore D. August 1986. "Multiple nuclear factors interact with the immunoglobulin enhancer sequences"; Cell. 46(5):705–16.</ref> 

== Structure  ==

There are five main proteins found that make up the mammalian NF-ϰB family, which are further sub-divided into two classes: I (NF-ϰB1 and NF-ϰB2 proteins) and II (RelA, Rel B and ''c''-Rel proteins).&nbsp;All of these proteins share a common [[Rel|Rel]] homology domain in the [[N-terminal|N-terminus]], but the Rel proteins have a transactivation domain in their [[C terminal|C termini]].<ref>Nabel GJ, Verma IM. November 1993. "Proposed NF-kappa B/I kappa B family nomenclature". Genes &amp;amp;amp; Development; 7 (11):2063.</ref> Whereas, the class I proteins are first translated from their genes as large precursors known as [[P105|p105]] and [[P100|p100]], which are processed via the [[Ubiquitin proteasome pathway|ubiquitin/proteasome pathway]] into their mature active subunits - [[P50|p50]] and [[P52|p52]] respectively. The functional structure of the NF-ϰB transcription [[Activator|activator]] is that of a [[Heterodimer|heterodimer]] between p50 or p52 and the Rel sub-family.&nbsp;There are two classes of NF-ϰB proteins. Those which fall into class I contain many [[Ankyrin|ankyrin]] repeats at the C-terminal of the protein, this means that the C-terminal is very long in comparison to those of class II. Due to these inhibiting factors, only when proteins of the first class form [[Dimer|dimers]] with class II Rel proteins can they activate transcription .<ref>Gilmore TD. October 2006. "Introduction to NF-kappaB: players, pathways, perspectives". Oncogene; 25(51):6680–4.</ref> The class II proteins have transcription [[Activation domain|activation domains]] in their C-terminals, the image on this link shows the difference clearly http://www.bu.edu/nf-kb/files/2011/02/figure-1.gif. (Ibid) 

== Function  ==

NF-ϰb has a role in preventing harm from environmental pressures to the cell,&nbsp;which can be in the form of bacterial or viral infection, [[Oxidative stress|oxidative stress]], DNA damage or [[Cytokine|cytokine]] production.&nbsp;NF-ϰB transcription factors play a role in various cellular processes, these include [[Apoptosis|apoptosis]] (cell death), cell growth and [[Immune responses|immune responses]]. In addition to this they can be prevalent in diseased states such as [[Cancer|cancer]], inflammatory and [[Autoimmune disease|autoimmune diseases]].<ref>Perkins ND. January 2007. "Integrating cell-signalling pathways with NF-kappaB and IKK function". Nature Reviews Molecular Cell Biology; 8(1): 49–62.</ref>&nbsp;NF-ϰB&nbsp;increases the&nbsp;amount of transcription that occurs by recruiting [[Histone Acetyltransferases|HATs]]&nbsp;and&nbsp;[[Swi/snf|Swi/Snf]] to help reconstruct the chromosome so they can reach DNA for transcription.&nbsp;Under normal conditions, NF-ϰB is mainly cytoplasmic but when control is lost it is found highly concentrated in the nucleus.<ref>Gilmore TD. October 2006. "Introduction to NF-kappaB: players, pathways, perspectives". Oncogene; 25(51):6680–4.</ref> 

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=== References  ===

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