Kwon sandbox: Difference between revisions

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==Research of Structure and Function==

C-~~myc is used~~ in ~~cell cycle entry, proliferation,~~ and ~~differentiation~~. C-~~myc also helps~~ to ~~bind~~ DNA ~~which activates transcription~~. ~~The~~ c-~~myc lives a very short life~~. ~~It is controlled by~~ the ~~level~~ and ~~temporal pattern~~ of ~~expression~~ of ~~their corresponding gene. Without C~~-~~myc an organism is unable~~ to ~~survive since there is nothing allowing cells~~ to ~~differentiate or proliferate. The organisms cannot survive after~~ the ~~pre~~-~~T-cell receptor proliferation is unable~~ to ~~be completed~~.

There are two main structures of the c-Myc proteins that are significant in its function. These are the Thr58 sight and the helix-loop-helix (HLH) motif surrounded by a basic amino acid region and a leucine zipper motif.

Kandil and colleagues speculated that the carboxyl terminus of the c-Myc protein had a similar structure to that of the helix-loop-helix family of DNA-binding proteins. Their research showed that the helix-loop-helix structure was in fact the DNA binding domain of c-Myc and were able to establish the corresponding binding sequence as GACCACGTGGTC. This sequence was found to be present in regulatory regions of genes during replication. They compared DNA binding of c-Myc to HLH protein TFEB. They found that the two proteins had the same inner nucleotides, providing significant evidence of the homology. Kandil and colleagues then placed spacing between half-sites of the DNA binding site. The inability of c-Myc to bind to the altered site provided evidence that c-Myc dimerizes when bound to DNA.

C-~~myc is also involved~~ in ~~the body's system of remembering past diseases~~. ~~T-cells help~~ the ~~body to remember diseases~~ it ~~has previously had~~. C-~~myc controls the regulation of T~~-~~cells~~. ~~Without C~~-~~myc the T~~-~~cells would not be triggered~~ to ~~multiply when a disease~~ that the ~~body has seen before infiltrates~~ the ~~body again~~.

Bahram and colleagues found that the mutation of Thr58 in c-Myc was prevalent in many cancers. They then researched the effect of Thr58 mutation and found that it was the ubiquitination site of the protein. Their in vitro experiment showed that c-Myc with Thr58 mutation had a longer turnover rate than wild type c-Myc. They also found that histadine-tagged ubiquitin octamers were unable to bind to Thr58 mutant c-Myc proteins but successfully did bind to wild type. This provided strong evidence that the site is indeed the ubiquitination site.

== References ==

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@@ Line 15: / Line 15: @@
 ==Research of Structure and Function==
-C-myc is used in cell cycle entry, proliferation, and differentiation. C-myc also helps to bind DNA which activates transcription. The c-myc lives a very short life. It is controlled by the level and temporal pattern of expression of their corresponding gene. Without C-myc an organism is unable to survive since there is nothing allowing cells to differentiate or proliferate. The organisms cannot survive after the pre-T-cell receptor proliferation is unable to be completed.
+There are two main structures of the c-Myc proteins that are significant in its function.  These are the Thr58 sight and the helix-loop-helix (HLH) motif surrounded by a basic amino acid region and a leucine zipper motif.
+Kandil and colleagues speculated that the carboxyl terminus of the c-Myc protein had a similar structure to that of the helix-loop-helix family of DNA-binding proteins.  Their research showed that the helix-loop-helix structure was in fact the DNA binding domain of c-Myc and were able to establish the corresponding binding sequence as GACCACGTGGTC.  This sequence was found to be present in regulatory regions of genes during replication.  They compared DNA binding of c-Myc to HLH protein TFEB.  They found that the two proteins had the same inner nucleotides, providing significant evidence of the homology.  Kandil and colleagues then placed spacing between half-sites of the DNA binding site.  The inability of c-Myc to bind to the altered site provided evidence that c-Myc dimerizes when bound to DNA.
-C-myc is also involved in the body's system of remembering past diseases.  T-cells help the body to remember diseases it has previously had.  C-myc controls the regulation of T-cells.  Without C-myc the T-cells would not be triggered to multiply when a disease that the body has seen before infiltrates the body again.
+Bahram and colleagues found that the mutation of Thr58 in c-Myc was prevalent in many cancers.  They then researched the effect of Thr58 mutation and found that it was the ubiquitination site of the protein.  Their in vitro experiment showed that c-Myc with Thr58 mutation had a longer turnover rate than wild type c-Myc.  They also found that histadine-tagged ubiquitin octamers were unable to bind to Thr58 mutant c-Myc proteins but successfully did bind to wild type.  This provided strong evidence that the site is indeed the ubiquitination site.
 == References ==