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== SKI protein == | == SKI protein == | ||
<Structure load='1sbx' size='500' frame='true' align='right' caption=' | <Structure load='1sbx' size='500' frame='true' align='right' caption='No caption inserted~~~~' scene='Insert optional scene name here' /> | ||
== Background == | == Background == | ||
The SKI protein was first identified as an oncoprotein. An oncoprotein is one that has the potential to cause abnormal cellular proliferation if mutated or if expressed in quantitative amounts. Although, for a time the method by which the SKI protein acquired such capabilities was unknown, it was recently discovered that SKI interacts with smad after stimulation by TGF-beta. TGF-beta are proteins directly associated with proliferation and cellular differentiation, while smads are transcription factors that transduce transforming growth factor-betar(TGF-beta) members to activate transcription. SKI blocks the activation of transcription witht eh smad complexes which makes the cells resistant to the inhibitory reactions of normal growth induced by TGF-beta. Note that the stimulation of TGF-beta may cause the rapid degradation of SKI. However, after a relatively brief amount of time its expression is strongly induced. <ref name="SKI protein"> Reed JA, Lin Q, Chen D, Mian IS, Medrano EE. SKI Pathways Inducing Progression of Human Melanoma. June 2005. http://www.ncbi.nlm.nih.gov/pubmed/15986136</ref>. | The SKI protein was first identified as an oncoprotein. An oncoprotein is one that has the potential to cause abnormal cellular proliferation if mutated or if expressed in quantitative amounts. Although, for a time the method by which the SKI protein acquired such capabilities was unknown, it was recently discovered that SKI interacts with smad after stimulation by TGF-beta. TGF-beta are proteins directly associated with proliferation and cellular differentiation, while smads are transcription factors that transduce transforming growth factor-betar(TGF-beta) members to activate transcription. SKI blocks the activation of transcription witht eh smad complexes which makes the cells resistant to the inhibitory reactions of normal growth induced by TGF-beta. Note that the stimulation of TGF-beta may cause the rapid degradation of SKI. However, after a relatively brief amount of time its expression is strongly induced. <ref name="SKI protein"> Reed JA, Lin Q, Chen D, Mian IS, Medrano EE. SKI Pathways Inducing Progression of Human Melanoma. June 2005. http://www.ncbi.nlm.nih.gov/pubmed/15986136</ref>. | ||
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== Clinical Applications == | == Clinical Applications == | ||
SKI has been linked to various types of cancer such as melanoma, esophageal cell carcinoma, cervical cancer and the process of tumor progresssion. The SKI oncoprotein has been demonstrated to assist tyrosine kinases to cause leukemia, recently it has been demonstrated that the protein also plays a regulatory role in several signal transduction pathways that are frequent targets for mutagenesis in human tumors. | SKI has been linked to various types of cancer such as melanoma, esophageal cell carcinoma, cervical cancer and the process of tumor progresssion. The SKI oncoprotein has been demonstrated to assist tyrosine kinases to cause leukemia, recently it has been demonstrated that the protein also plays a regulatory role in several signal transduction pathways that are frequent targets for mutagenesis in human tumors. Much research performed on the SKI protein is based on the role it plays in the proliferation of cells in human melanoma<ref name="ca"> Marcelain K, Hayman MJ. Fall 2005. The Ski oncoprotein is upregulated by localized centrosomes and mitotic spindle during metosis. http://www.nature.com/onc/journal/v24/n27/full/1208631a.html</ref>. | ||
== References == | == References == | ||
<references/> | <references/> | ||