DIS3L2: Uridiylation Control of the Lin28-Let-7 Differentiation Pathway

Thu, 06/20/2013 - 11:43

The Lin28-Let-7 stem cell differentiation regulatory pathway is responsible for maintaining stem cell pluripotency. Specifically, Lin28 causes uridiylation of the let-7 miRNA precursor, which prevents differentiation processing by Dicer. Instead, the Uridylated let-7 is degraded by a previously unidentified exonuclease protein. In the article A role for the Perlman syndrome exonuclease Dis3l2 in the Lin28-let-7 pathway” HM Chang, et al. used Novus’ Dis3l2 Antibody (NBP1-84740) to identify Dis3l2 as the exonuclease responsible for uridylated let-7 degradation.  Interestingly, Dis3l2 binds several proteins previously implicated in Perlman Sydrome.

The implications of this finding are two-fold: (1) The data suggests that Dis3l2 helps maintain pluripoentcy in stem cells, and (2) although speculative, the Lin28-let-7 pathway may be relevant to Perlman Sydrome and cancer.  Additional research is now necessary to confirm the role for Dis3l2 in maintaining pluripotency, as well as to expand the link between this exonuclease and other diseases. For further information, please read the full article available through Nature.

To promote additional research on the Lin28-Let-7 stem cell differentiation pathway we are offering antibodies to each of the targets examined in this article at 20% off. Please select from any of the antibodies available through the following links, and enter code DIS3L2 at checkout to redeem your discount:

Dis3l2 Antibody (NBP1-84740)
Lin28 Antibody (NBP1-49537)
DICER Antibody (NBP1-71691)
Wilm’s Tumor 1 Antibody (NB110-60011)
ZCCHC6 Antibody (NBP1-82257)
ZCCHC11 Antibody (NBP1-83027)

Additionally, you may browse a complete list of our stem cell marker reagents.

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