proto-oncogene activation
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The proto-oncogene can become an oncogene by a relatively small modification of its original function. There are three basic methods of activation:
A mutation within a proto-oncogene, or within a regulatory region (for example the promoter region), can cause a change in the protein structure, causing
an increase in protein (enzyme) activity
a loss of regulation
An increase in the amount of a certain protein (protein concentration), caused by
an increase of protein expression (through misregulation)
an increase of protein (mRNA) stability, prolonging its existence and thus its activity in the cell
gene duplication (one type of chromosome abnormality), resulting in an increased amount of protein in the cell
A chromosomal translocation (another type of chromosome abnormality)
There are 2 different types of chromosomal translocations that can occur:
translocation events which relocate a proto-oncogene to a new chromosomal site that leads to higher expression
translocation events that lead to a fusion between a proto-oncogene and a 2nd gene (this creates a fusion protein with increased cancerous/oncogenic activity)
the expression of a constitutively active hybrid protein. This type of mutation in a dividing stem cell in the bone marrow leads to adult leukemia
Philadelphia Chromosome is an example of this type of translocation event. This chromosome was discovered in 1960 by Peter Nowell and David Hungerford, and it is a fusion of parts of DNA from chromosome 22 and chromosome 9. The broken end of chromosome 22 contains the "BCR" gene, which fuses with a fragment of chromosome 9 that contains the "ABL1" gene. When these two chromosome fragments fuse the genes also fuse creating a new gene: "BCR-ABL". This fused gene encodes for a protein that displays high protein tyrosine kinase activity (this activity is due to the "ABL1" half of the protein). The unregulated expression of this protein activates other proteins that are involved in cell cycle and cell division which can cause a cell to grow and divide uncontrollably (the cell becomes cancerous). As a result, the Philadelphia Chromosome is associated with Chronic Myelogenous Leukemia (as mentioned before) as well as other forms of Leukemia.[13]
The expression of oncogenes can be regulated by microRNAs (miRNAs), small RNAs 21-25 nucleotides in length that control gene expression by downregulating them.[14] Mutations in such microRNAs (known as oncomirs) can lead to activation of oncogenes.[15] Antisense messenger RNAs could theoretically be used to block the effects of oncogenes.
http://shomusbiology.weebly.com/
Download the study materials here-
http://shomusbiology.weebly.com/bio-m...
Source of the article published in description is Wikipedia. Thanks to original content developers.
Link- http://en.wikipedia.org/wiki/Main_Page
The proto-oncogene can become an oncogene by a relatively small modification of its original function. There are three basic methods of activation:
A mutation within a proto-oncogene, or within a regulatory region (for example the promoter region), can cause a change in the protein structure, causing
an increase in protein (enzyme) activity
a loss of regulation
An increase in the amount of a certain protein (protein concentration), caused by
an increase of protein expression (through misregulation)
an increase of protein (mRNA) stability, prolonging its existence and thus its activity in the cell
gene duplication (one type of chromosome abnormality), resulting in an increased amount of protein in the cell
A chromosomal translocation (another type of chromosome abnormality)
There are 2 different types of chromosomal translocations that can occur:
translocation events which relocate a proto-oncogene to a new chromosomal site that leads to higher expression
translocation events that lead to a fusion between a proto-oncogene and a 2nd gene (this creates a fusion protein with increased cancerous/oncogenic activity)
the expression of a constitutively active hybrid protein. This type of mutation in a dividing stem cell in the bone marrow leads to adult leukemia
Philadelphia Chromosome is an example of this type of translocation event. This chromosome was discovered in 1960 by Peter Nowell and David Hungerford, and it is a fusion of parts of DNA from chromosome 22 and chromosome 9. The broken end of chromosome 22 contains the "BCR" gene, which fuses with a fragment of chromosome 9 that contains the "ABL1" gene. When these two chromosome fragments fuse the genes also fuse creating a new gene: "BCR-ABL". This fused gene encodes for a protein that displays high protein tyrosine kinase activity (this activity is due to the "ABL1" half of the protein). The unregulated expression of this protein activates other proteins that are involved in cell cycle and cell division which can cause a cell to grow and divide uncontrollably (the cell becomes cancerous). As a result, the Philadelphia Chromosome is associated with Chronic Myelogenous Leukemia (as mentioned before) as well as other forms of Leukemia.[13]
The expression of oncogenes can be regulated by microRNAs (miRNAs), small RNAs 21-25 nucleotides in length that control gene expression by downregulating them.[14] Mutations in such microRNAs (known as oncomirs) can lead to activation of oncogenes.[15] Antisense messenger RNAs could theoretically be used to block the effects of oncogenes.
11 سال پیش
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