Contact information
Research groups
Khatoun Al Moussawi
Post-doctoral Fellow
I received my PhD from the Faculty of Medicine, University of Aix-Marseille II, France. Funded by an Infectiopole Sud Fellowship, my research focused on new insights into Whipple's disease and Tropheryma whipplei infections. After this, I did postdoctoral research in infectious disease and microbial pathogenesis at Yale University, USA. I studied the innate immune recognition of Pseudomonas aeruginosa and I characterised a novel human syndrome of enterocolitis and autoinflammation, caused by mutation of the NLRC4 inflammasome.
I am currently a Postdoctoral Researcher at the Ludwig Institute for Cancer Research, Oxford University, UK, where I am a member of Xin Lu’s lab. Our research focuses on studying the regulation of the tumour suppressor p53, which is the most mutated gene in human cancers with a vital role in protection against tumorigenesis. p53 does not act alone: there are several signalling pathways and important regulators that interact with the p53 axis, including the ASPP family of proteins, a family of evolutionarily conserved regulators of p53. ASPP proteins play important roles in p53 regulation, with ASPP1/ ASPP2 activating p53 and iASPP inhibiting p53.
My research is broadly focused on understanding the regulation of p53 in human haematopoietic stem cells and in investigating p53 mutational status in haematological malignancies in relation to the expression levels and functions of the ASPP family of proteins. I am also interested in investigating the crosstalk between p53 regulators, infection and inflammation.
Recent publications
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Deficiency of factor-inhibiting HIF creates a tumor-promoting immune microenvironment
Journal article
Ma J. et al, (2024), Proceedings of the National Academy of Sciences, 121
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Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis
Journal article
Al Moussawi K. et al, (2022), Cell Reports, 41, 111503 - 111503
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NAIP proteins are required for cytosolic detection of specific bacterial ligands in vivo
Journal article
Rauch I. et al, (2016), Journal of Experimental Medicine, 213, 657 - 665
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Distinct Contributions of Interleukin-1α (IL-1α) and IL-1β to Innate Immune Recognition of Pseudomonas aeruginosa in the Lung
Journal article
Al Moussawi K. and Kazmierczak BI., (2014), Infection and Immunity, 82, 4204 - 4211
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Mutation of NLRC4 causes a syndrome of enterocolitis and autoinflammation
Journal article
Romberg N. et al, (2014), Nature Genetics, 46, 1135 - 1139