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hashim-ali

Dr Hashim Ali

Research Associate

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Biography

Dr Hashim Ali is a Research Associate within the School of Cardiovascular Medicine & Sciences at James Black Centre, King’s College London. He did his PhD in the lab of Prof. Mauro Giacca at International Center for Genetic Engineering and Biotechnology (ICGEB), Trieste, ITALY. During his PhD, he contributed to the identification of the host factors regulating HIV-1 integration, transcription and integrase protein stability. He also contributed to show for the first time the topological location of the integration HIV-1 inside the cell nucleus. In his PhD, he identified that the host ubiquitin E3 ligase TRIM33, degrades HIV-1 integrase. Sideways, he also worked on a project involved in the identification and characterization of the mechanisms of extracellular secretion of the HIV-1 Tat protein and identified that the cellular Na+K+ATPase alpha1 subunit plays a key role in non-canonical extracellular release of Tat protein. His entire work is well presented and a significant advancement in the field that identifies the important role of the cellular factors regulating HIV-1 integration. After gaining expertise in ubiquitin-proteasomal degradation pathway, he became interested in identifying endogenous pathways/human miRNAs regulating cardiomyocyte proliferation that could potentially be used as cardiac regenerative therapeutics. This led him to join the group of Prof. Mauro Giacca at ICGEB, Trieste, ITALY and later at King’s College London, UK. During his early postdoctoral training, he studied in depth the role of human miRNAs/endogenous pathways regulating cardiac regeneration. At King’s College London, his research interest includes investigating the novel ubiquitin-conjugation factors capable of modulating cardiomyocyte proliferation. He is also interested in the understanding of the crucial endogenous pathways regulating cardiac regeneration and how posttranslational modifications of proteins and remodeling of cardiac cytoskeletons contribute to cardiac dysfunction.