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Maria Pia Arrate

Researcher at Vanderbilt University

Publications -  16
Citations -  623

Maria Pia Arrate is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Venetoclax & Myeloid leukemia. The author has an hindex of 9, co-authored 16 publications receiving 469 citations. Previous affiliations of Maria Pia Arrate include Vanderbilt University Medical Center.

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A Novel MCL1 Inhibitor Combined with Venetoclax Rescues Venetoclax-Resistant Acute Myelogenous Leukemia.

TL;DR: VU661013 is described, a novel, potent, selective MCL1 inhibitor that destabilizes BIM/MCL1 association, leads to apoptosis in AML, and is active in venetoclax-resistant cells and patient-derived xenografts.
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MicroRNA-31 initiates lung tumorigenesis and promotes mutant KRAS-driven lung cancer

TL;DR: It is determined that miR-31 is overexpressed in human lung adenocarcinoma and this overexpression independently correlates with decreased patient survival and is distinguished as a driver of lung tumorigenesis that promotes mutant KRAS-mediated oncogenesis and reveals that mi R-31 directly targets and reduces expression of negative regulators of RAS/MAPK signaling.
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MicroRNA Biogenesis Is Required for Myc-Induced B-Cell Lymphoma Development and Survival

TL;DR: It is reported that a haploinsufficiency of Dicer in B cells failed to promote B-cell malignancy or accelerate Myc-induced B- cell lymphomagenesis in mice, and Dicer ablation was strongly selected against during Myc's B-cells lymphoma development.
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Cutting Edge: K63-Linked Polyubiquitination of NEMO Modulates TLR Signaling and Inflammation In Vivo

TL;DR: It is demonstrated that NF-κB and MAPK pathways are largely unaffected in primary cells from mice harboring a ubiquitination-defective form of NEMO, NemO-KR, which is more resistant to LPS-induced endotoxic shock than wild-type animals.
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Mdmx promotes genomic instability independent of p53 and Mdm2.

TL;DR: A novel p53- and Mdm2-independent oncogenic function of Mdmx is revealed that provides new insight into the many cancers that overexpress MDMx and resulted in delayed DNA repair and increased genome instability and transformation independent of p53 and MDM2.