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Ekaterina Bobrovnikova-Marjon

Researcher at University of Pennsylvania

Publications -  14
Citations -  2432

Ekaterina Bobrovnikova-Marjon is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Unfolded protein response & Endoplasmic reticulum. The author has an hindex of 12, co-authored 14 publications receiving 2094 citations. Previous affiliations of Ekaterina Bobrovnikova-Marjon include Agios Pharmaceuticals.

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The GCN2-ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation

TL;DR: It is concluded that the GCN2‐eIF2α‐ATF4 pathway is critical for maintaining metabolic homeostasis in tumour cells, making it a novel and attractive target for anti‐tumour approaches.
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PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage

TL;DR: The data reveal that PERK-dependent signaling is used during both tumor initiation and expansion to maintain redox homeostasis, thereby facilitating tumor growth.
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PERK integrates autophagy and oxidative stress responses to promote survival during extracellular matrix detachment.

TL;DR: It is shown that the endoplasmic reticulum kinase PERK facilitates survival of ECM-detached cells by concomitantly promoting autophagy, ATP production, and an antioxidant response, and it is proposed that the normal proautophagic and antioxidant PERK functions may be hijacked to promote the survival ofECM- Detached tumor cells in DCIS lesions.
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HIF2α-Dependent Lipid Storage Promotes Endoplasmic Reticulum Homeostasis in Clear-Cell Renal Cell Carcinoma

TL;DR: It is demonstrated that Hif2α promotes lipid storage, ER homeostasis, and cell viability in ccRCC via upregulation of the LD coat protein PLIN2, revealing a novel function for the well-documented "clear-cell" phenotype and identifying ER stress as a targetable vulnerability created by HIF2α/PLIN2 suppression in this common renal malignancy.
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PERK-dependent regulation of lipogenesis during mouse mammary gland development and adipocyte differentiation

TL;DR: Loss of PERK inhibits expression of FAS, ACL, and SCD1 in immortalized murine embryonic fibroblasts when cultured under conditions favoring adipocyte differentiation, implicate PERK as a physiologically relevant regulator of the lipogenic pathway.