horsepuckey...In both of these studies they are referring to SNP's in the Introns of the genes. I have realized for years that you have no idea what you're talking about, but these posts pretty much confirm it.
Here you go buckshot:
Intron
Introns are sequences of "junk" DNA found in the middle of gene sequences. These sequences are excised before the mRNA is translated into a protein. The function of introns is not known.
This from the study discussion:
The SNPs in intron 2 reside in a region of marked DNA conservation between mouse and human. Such conserved nongenic sequences were recently proposed as additional regulatory elements (29). Indeed, SNPs 2351, 2399, and 2949 alter putative binding sites for transcription factors TATA, MZF1 and P300, and SP1, respectively (Fig. 3, online appendix). Of these, SNP 2399 is predicted to abolish binding for MZF1 and P300 and SNP 2949 is predicted to abolish binding for SP1 transcription factors. Thus, this region might alter CASQ1 or perhaps PEA15 regulation and contribute to diabetes risk.
In other words, they are suggesting that the subject SNP's, within intron i.e. "junk" region 2 serve as some sort of regulatory element. They don't have to "code" to impact protein synthesis. The authors are in fact suggesting that their effect may be through a "regulation" of the coding process itself.
Now, by my read Johnnyfiber has it exactly correct and you have it completely wrong. How about a legitimate apology, rather than an attempt to lie your way out of it.
Later,
W2P
