Anyway these guys pulled out an interesting protein called Lin-28 in a screen for regulators of Let-7 processing in embryonic stem cells. In stem cells, and presumably cancer cells as well, the idea is that Lin28 binds to the primary Let-7 transcript and prevents processing to the active form. Genes that would otherwise be regulated by Let-7 can therefore be expressed and pluripotency/proliferation carries on. In differentiated cells, Lin-28 is down-regulated, freeing Let-7 to go about it's business repressing it's targets. Or so the story goes.
We already knew that Lin-28 was an RNA-binding protein of developmental significance, so this new finding makes a lot of sense. Palazzo has been drooling all over this paper, and he's particularly worked up about the fact the Lin-28 was also recently identified as one of the magic factors that can reprogram adult somatic cells into pluripotent, embryonic-like stem cells. Read what he has to say for more on this. I find it interesting to note that Lin-28 can be found in P-bodies, cytoplasmic sites of RNA processing that seem to be part of the whole miRNA game (see also here for recent developments in the miRNA-P-body connection).
Anyway, that's enough blathering for now on the clearly trivial research that is being done over at the Harvard Medical School.
1 comments:
Let-7 is your daddy.
Here it is curing mouse models of lung cancer.
And here aswell.
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