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Hasan Rajabi

Researcher at Harvard University

Publications -  69
Citations -  3401

Hasan Rajabi is an academic researcher from Harvard University. The author has contributed to research in topics: MUC1 & Gene silencing. The author has an hindex of 34, co-authored 67 publications receiving 2640 citations. Previous affiliations of Hasan Rajabi include Dana Corporation & Northwestern University.

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MUC1 oncoprotein activates the IκB kinase β complex and constitutive NF-κB signalling

TL;DR: In this paper, it was shown that MUC1 is associated with constitutive activation of NF-κB p65 in human carcinoma cells, and that the activation of IKKβ is dependent on TAK1 and TAB2.
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Dependence on the MUC1-C Oncoprotein in Non–Small Cell Lung Cancer Cells

TL;DR: It is shown that inhibition of MUC1-C with cell-penetrating peptides blocks this interaction with PI3K p85 and suppresses constitutive phosphorylation of Akt and its downstream effector, mTOR.
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MUC1-C Induces PD-L1 and Immune Evasion in Triple-Negative Breast Cancer.

TL;DR: It is reported that genetic or pharmacological targeting of the oncogenic M UC1 subunit MUC1-C is sufficient to suppress PD-L1 expression in TNBC cells, and this finding offers a rationale to target MUC-C as a novel immunotherapeutic approach for TNBC treatment.
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MUC1-mediated induction of myeloid-derived suppressor cells in patients with acute myeloid leukemia

TL;DR: It is demonstrated that AML EVs are taken-up myeloid progenitor cells, resulting in the selective proliferation of MDSCs in comparison with functionally competent antigen-presenting cells, and the microRNA miR34a acts as the regulatory mechanism by which MUC1 drives c-myc expression in AML cells and EVs.
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Functional interactions of the cystine/glutamate antiporter, CD44v and MUC1-C oncoprotein in triple-negative breast cancer cells.

TL;DR: It is shown that silencing MUC1-C is associated with decreases in xCT expression in TNBC cells and that targeting this novel MUC2-C/xCT pathway could represent a potential therapeutic approach for promoting TNBC cell death.