Researchers at St. Jude used a mouse model to show that the Ulk kinase gene, which encodes a protein that drives some forms of autophagy, participates in removal of excess free alpha globin (SJ-18-0004). This discovery can lead to new unanticipated treatment applications for old and new drugs for research in a variety of disease indications. Contact us if interested in licensing these mice with the following genotype: Ulk1-/- Ulk2 flox/-.
- The specimens develop inclusion-body myopathy and are useful to clinical development of this disease. Moreover, this model may prove useful for preclinical development for other diseases relating to Ulk function and/or autophagy defects.
- The Ulk1/2-hypomorph specimens and derived cells are useful in the development of ULK1/2 agonists or treatments aimed at increasing Ulk2 expression. Augmentation of Ulk function is a promising strategy for the treatment of several types of diseases, including but not limited to protein aggregation diseases and certain genetic syndromes such as patients with VCP mutations.
Ulk kinase gene, autophagy, excess free alpha globin, inclusion-body myopathy, VCP mutations.
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