Ras: Difference between revisions
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The Ras protein is a [[Monomeric G-protein|monomeric G-protein]] with weak [[GTPase|GTPase]] [[Enzyme|enzyme]] activity. It is a [[Signal-transducer protein|signal-transducer protein]] for growth factors and therefore it helps to transfer signals from cell-surface [[Receptor Tyrosine Kinase|Receptor Tyrosine Kinase]] (RTK) receptors to the [[Nucleus|nucleus]] <ref>Alberts, B, et al, 2008. Molecular Biology of the Cell. 5th ed. United States of America: Garland Science.</ref>.<br> | |||
=== Active and Inactive forms of Ras === | |||
Ras is in its inactive form when it is bound to [[GDP|GDP]], and becomes active once GDP has been exchanged for a [[GTP|GTP]] molecule. This reaction is initiated by the action of a specific signal molecule binding to a [[RTK receptor|RTK receptor]] on the cell membrane. The activated RTK has intrinsic [[Kinase|kinase]] activity, and this leads to [[Phosphorylation|phosphorylation]] of docking proteins at the RTK domains. The adaptor protein [[Grb-2|Grb-2]] mediates the reaction between the RTK and Ras [[GEF|GEF]] (GEF binds indirectly to RTK) , which exchanges GDP for GTP, acvtivating Ras which can transmit of a signal along multiple pathways. RTK is not the only way to activate Ras. The Ras GEF found in the brain for example, can bind to the [[GPCR|GPCR and]] thus activate the Ras without the RTK. The inactivation of Ras is caused by the hydrolysis of GTP and it is mediated by Ras GAP. If the GTP bound at Ras cannot be [[Hydrolysis|hydrolysed]] then it would cause Ras to stay in an active form and thus lead to [[Cancer|cancer]]<ref>2. Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walter, P. . (2008). Signalling through enzyme-coupled cell-surface receptors. In: Anderson, M. and Granum, S. Molecular Biology of The Cell. 5th ed. USA: Garland Science. 927.</ref><ref>Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walter, P. . (2008). Signalling through enzyme-coupled cell-surface receptors. In: Anderson, M. and Granum, S. Molecular Biology of The Cell. 5th ed. USA: Garland Science. 927.</ref>.<br> | |||
=== References<br> === | |||
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Latest revision as of 06:48, 26 November 2014
The Ras protein is a monomeric G-protein with weak GTPase enzyme activity. It is a signal-transducer protein for growth factors and therefore it helps to transfer signals from cell-surface Receptor Tyrosine Kinase (RTK) receptors to the nucleus [1].
Active and Inactive forms of Ras
Ras is in its inactive form when it is bound to GDP, and becomes active once GDP has been exchanged for a GTP molecule. This reaction is initiated by the action of a specific signal molecule binding to a RTK receptor on the cell membrane. The activated RTK has intrinsic kinase activity, and this leads to phosphorylation of docking proteins at the RTK domains. The adaptor protein Grb-2 mediates the reaction between the RTK and Ras GEF (GEF binds indirectly to RTK) , which exchanges GDP for GTP, acvtivating Ras which can transmit of a signal along multiple pathways. RTK is not the only way to activate Ras. The Ras GEF found in the brain for example, can bind to the GPCR and thus activate the Ras without the RTK. The inactivation of Ras is caused by the hydrolysis of GTP and it is mediated by Ras GAP. If the GTP bound at Ras cannot be hydrolysed then it would cause Ras to stay in an active form and thus lead to cancer[2][3].
References
- ↑ Alberts, B, et al, 2008. Molecular Biology of the Cell. 5th ed. United States of America: Garland Science.
- ↑ 2. Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walter, P. . (2008). Signalling through enzyme-coupled cell-surface receptors. In: Anderson, M. and Granum, S. Molecular Biology of The Cell. 5th ed. USA: Garland Science. 927.
- ↑ Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walter, P. . (2008). Signalling through enzyme-coupled cell-surface receptors. In: Anderson, M. and Granum, S. Molecular Biology of The Cell. 5th ed. USA: Garland Science. 927.