A study from the Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Boston Children’s Hospital and Dana Farber Cancer Institute, Boston, Massachusetts, USA shows that “The Lin28/let-7 axis regulates glucose metabolism.” This study was published in the 30 September 2011 issue of the Journal “Cell” [I.F: 33.116] by Prof Daley GQ, Zhu H, and others.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Regenerative therapy for DM: HMGA2 promotes an insulin-sensitized state via up regulation of reprogramming protein Lin28
Significance: Prof. Daley GQ and his team members had shown that loss of Lin28 in muscles promotes insulin resistance and glucose intolerance. This study suggests, for the first time, that HMGA2, by increasing the expression of its target gene, it may increase the expression of RNA-binding protein Lin-28. Thereby, it may (1) increase the expression of IGF1R, INSR, and IRS2; (2) enhance tissue repair; (3) promote youthful regenerative capacity; and (4) promote insulin sensitivity. Thus, pharmacological formulations encompassing ” HMGA2 activators or small molecule compounds that activate both HMGA2 and Lin28″ may be used to treat DM.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Web: http://genomediscovery.org
Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/
Undisclosed information: How HMGA2 increases the expression of Lin28
To cite: Boominathan, Regenerating the lost pancreatic β-cells in Diabetic patients: HMGA2 promotes an insulin-sensitized state via up regulation of reprogramming protein Lin28, 18/April/2015, 7.55 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Courtesy: When you cite drop us a line at info@genomediscovery.org
* Research cooperation