Tuesday, August 25, 2009

CCR3, GATA-1, Blah blah blaaaaaAAAAHHH!!

This post is seriously for my own good - I honestly can't find anyone interested in reading what I'm about to write, I know how people spazz out when they start reading scientific jargon...just want to keep a brief record of what I'm learning in these articles.

Latest article was entitled Analysis of the CCR3 promoter reveals a regulatory region in exon 1 that binds GATA-1...told you it's a bit on the drier side of biomed articles. Actually, it's not that it's boring, I just hate reading these articles based heavily on molecular biology and genetics that don't explicitly tie into some pathology. I mean, the article delves into analyzing the regulation and expression of the CCR3 gene among various cell lineages, but doesn't go one step further into hypothesizing implications in a real world context (i.e. the role of CCR3 in HIV-1 infection), leaving me thirsty for a little bit more...

So yeah, the article starts by stating that while many cells in our bodies express CCR3, the main ones that accumulate after administration of eotaxin are namely eosinophils. This is somewhat unexpected, as one would expect that all cells expressing this receptor would bind to the specified ligand. Logically, one would suspect that there is some sort of differential regulation occurring, where eosinophils are expressing CCR3 and for some reason these other cells aren't, right? In short, researchers found that TFs, namely GATA-1, bind to exon 1 in the gene, thus regulating its transcription. Findings were reinforced using transgenic mice.

Fun, fun, fun. I've been working on annotating this one article for the past 2 weeks. Thankfully, the next one looks a bit more interesting. The first set of articles dealt extensively with research in arthritis using mice models of AA to relate to RA in humans. This next set of articles seems to deal with different features of HIV infection - yay! I think HIV infection and progression of the disease is genetically and cellularly fascinating! Yes, I admit I have transformed into a huge nerd.


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