MAP kinase: Difference between revisions

From The School of Biomedical Sciences Wiki
Jump to navigation Jump to search
No edit summary
Nnjm2 (talk | contribs)
No edit summary
 
Line 1: Line 1:
Mitogen-activated protein kinases (MAPKs) contribute to a variety of cellular processes such as [[Gene expression|gene expression]] and [[Apoptosis|apoptosis]] via cell signalling pathways&nbsp;<ref>Ralph A. Bradshaw, Edward A. Dennis Academic Press, 3 Nov 2009. Page 1303-1304</ref><ref>Pearson G, Robinson F, Beers Gibson T, Xu BE, Karandikar M, Berman K and Cobb MH. (2001). Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions. Endocrine Reviews. 22 (2), p153-183.</ref>.  
Mitogen-activated protein kinases (MAPKs) contribute to a variety of cellular processes such as [[Gene expression|gene expression]] and [[Apoptosis|apoptosis]] via cell signalling pathways&nbsp;<ref>Ralph A. Bradshaw, Edward A. Dennis Academic Press, 3 Nov 2009. Page 1303-1304</ref><ref>Pearson G, Robinson F, Beers Gibson T, Xu BE, Karandikar M, Berman K and Cobb MH. (2001). Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions. Endocrine Reviews. 22 (2), p153-183.</ref>.  


== Ras-MAP-kinase signalling pathway  ==
=== Ras-MAP-kinase signalling pathway  ===


Ras, the [[Monomeric G-protein|monomeric G-protein]], activates the MAP kinase pathway. This is made up of three protein kinases: MAP kinase kinase kinase ([[Raf|Raf]]), MAP kinase kinase ([[Mek|Mek]]) and MAP kinase ([[Erk|Erk]]). The Raf molecule acquires an activation signal from Ras, causing it to phosphorylate and activate the next kinase in the series, Mek. This produces a downstream phosphorylation cascade. Once the final MAP kinase (Erk) has been activated, other proteins such as transcription factors and other protein kinases can be activated, leading to changes in gene expression and protein activity<ref>Bruce Alberts. (2015). Chapter 15: Cell signalling. In: Molecular Biology of the Cell. New York: Garland Science. p855-856.</ref>.&nbsp;  
Ras, the [[Monomeric G-protein|monomeric G-protein]], activates the MAP kinase pathway. This is made up of three protein kinases: MAP kinase kinase kinase ([[Raf|Raf]]), MAP kinase kinase ([[Mek|Mek]]) and MAP kinase ([[Erk|Erk]]). The Raf molecule acquires an activation signal from Ras, causing it to phosphorylate and activate the next kinase in the series, Mek. This produces a downstream phosphorylation cascade. Once the final MAP kinase (Erk) has been activated, other proteins such as transcription factors and other protein kinases can be activated, leading to changes in gene expression and protein activity<ref>Bruce Alberts. (2015). Chapter 15: Cell signalling. In: Molecular Biology of the Cell. New York: Garland Science. p855-856.</ref>.&nbsp;  


== References  ==
=== References  ===


<references />
<references />

Latest revision as of 13:12, 30 November 2015

Mitogen-activated protein kinases (MAPKs) contribute to a variety of cellular processes such as gene expression and apoptosis via cell signalling pathways [1][2].

Ras-MAP-kinase signalling pathway

Ras, the monomeric G-protein, activates the MAP kinase pathway. This is made up of three protein kinases: MAP kinase kinase kinase (Raf), MAP kinase kinase (Mek) and MAP kinase (Erk). The Raf molecule acquires an activation signal from Ras, causing it to phosphorylate and activate the next kinase in the series, Mek. This produces a downstream phosphorylation cascade. Once the final MAP kinase (Erk) has been activated, other proteins such as transcription factors and other protein kinases can be activated, leading to changes in gene expression and protein activity[3]

References

  1. Ralph A. Bradshaw, Edward A. Dennis Academic Press, 3 Nov 2009. Page 1303-1304
  2. Pearson G, Robinson F, Beers Gibson T, Xu BE, Karandikar M, Berman K and Cobb MH. (2001). Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions. Endocrine Reviews. 22 (2), p153-183.
  3. Bruce Alberts. (2015). Chapter 15: Cell signalling. In: Molecular Biology of the Cell. New York: Garland Science. p855-856.