DOWNREGULATION OF miR-7 FOR PROMOTION OF BETA CELL DIFFERENTIATION AND INSULIN PRODUCTION
AssigneeYeda Research and Development Co. Ltd.
InventorsEran Hornstein, Sharon Kredo-Russo
Life of this patent
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Abstract
A method of ex-vivo increasing insulin content in beta cells or stem cells is disclosed. The method comprising contacting the beta cells or stem cells with an agent for downregulating an activity or expression of miR-7, thereby increasing the insulin content in the beta cells or stem cells.
Claims35
A method of ex-vivo increasing insulin content in beta cells or stem cells, the method comprising contacting said beta cells or stem cells with an agent for downregulating an activity or expression of miR-7, thereby increasing said insulin content in said beta cells or stem cells.
An isolated population of cells comprising an exogenous agent for downregulating an activity or expression of miR-7, wherein said cells secrete insulin.
5-6. (canceled)
A method of treating a medical condition associated with an insulin deficiency in a subject in need thereof, the method comprising administering to the subject an agent for downregulating an activity or expression of miR-7, thereby treating the medical condition associated with the insulin deficiency.
10-11. (canceled)
15-16. (canceled)
A method of increasing insulin content in beta cells or stem cells, the method comprising expressing in said beta cells or stem cells a target gene of miR-7 selected from the group consisting of epidermal growth factor receptor (EGFR), insulin-degrading enzyme (IDE), Kruppel-like factor 4 (KLF4), GLI family zinc finger 3 (GLI3), insulin receptor substrate 1 (IRS1), Sp1 transcription factor (SP1), O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase) (OGT), insulin-like growth factor 1 receptor (IGF1R) and one cut homeobox 2 (ONECUT2), thereby increasing said insulin content in said beta cells or stem cells.
22-25. (canceled)
An isolated population of beta cells or stem cells exogenously expressing a target gene of miR-7 selected from the group consisting of epidermal growth factor receptor (EGFR), insulin-degrading enzyme (IDE), Kruppel-like factor 4 (KLF4), GLI family zinc finger 3 (GLI3), insulin receptor substrate 1 (IRS1), Sp1 transcription factor (SP1), O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase) (OGT), insulin-like growth factor 1 receptor (IGF1R) and one cut homeobox 2 (ONECUT2).
(canceled)
32-33. (canceled)
37-38. (canceled)
Dependencies are inferred from the claim text.