Upcoming Projects

International

Qatar University Biomedical Research Center

  1. Clinical Protective Effect of SGLT2 Inhibitors in Diabetes Induced Cardiovascular Diseases: Proposed Novel Mechanisms of Action – A Reverse Translational Study, QNRF – National Priority Research Program.
  2. Investigation of diabetes-associated and non-diabetic heart failure in zebrafish and investigation of the effects of sodium-glucose cotransporter-2 (SGLT2) inhibition on cardiac function using genetic (SGLT2 KO fish creation) and pharmaceutical approaches. In this project, the creation of KO fish and the production of homozygous mutant fish will be carried out under the responsibility of our laboratory.
  3. As the continuation of the project numbered TÜBİTAK-1001 214S174; analysis of swimming behavior and evaluation of cardiac function in adult desmakg155/kg155 and desmakg155/kg155:desmb-KO fish; These fish were produced by our laboratory, but collaboration is made at the Qatar University Biomedical Research Center because of the experimental infrastructure for analysis of swimming behavior and heart function in adult fish.

Interinstitutional

  1. Gazi University Medical Genetics; Demonstrating the status of being the gene responsible for the phenotype by KO with CRISPR-Cas9 of the candidate gene that may be associated with LGMD2.
  2. Ankara University Faculty of Medicine Geriatrics; Investigation of the relationship between muscle and bone in zebrafish at the molecular level in order to clarify the relationship between sarcopenia and osteoporosis.
  3. University of Health Sciences, Gulhane Faculty of Medicine. Department of Medical Biology; Creating a zebrafish model of LGMD-R17 (Limb girdle muscular dystrophy R17 locus-plectin 1f), (LGMD-R17 locus is the locus that the PhD student of PI identified it in her thesis project and for the first time in the literature, a disease which is caused due to an isoform-specific mutation.)

Institutional

  1. Hacettepe University, Pediatric Nephrology; KO and phenotypic evaluation of ctns gene causing cystinosis disease via CRISPR-Cas9 in zebrafish
  2. Correction of the 32 base pair duplication detected in the beta-sarcoglycan gene in the LGMD2E patient for preclinical molecular therapy using the CRISPR-Prime Editing method in the patient’s immortalized myoconverted fibroblast cells.