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Rachana Garg

Researcher at University of Pennsylvania

Publications -  33
Citations -  1000

Rachana Garg is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Cancer & Carcinogenesis. The author has an hindex of 12, co-authored 21 publications receiving 787 citations. Previous affiliations of Rachana Garg include Department of Biotechnology & Cancer Research Institute.

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Protein kinase C and cancer: what we know and what we do not

TL;DR: Unraveling the enormous complexity in the mechanisms by which PKC isozymes have an impact on tumorigenesis and metastasis is key for reassessing their potential as pharmacological targets for cancer treatment.
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Dietary curcumin modulates transcriptional regulators of phase I and phase II enzymes in benzo[a]pyrene-treated mice: mechanism of its anti-initiating action.

TL;DR: Curcumin exhibits anti-initiating effects via modulating the transcriptional regulators of phase I and phase II enzymes in mice through inhibition of B[a]P-induced enzyme activity, protein and messenger RNA levels of cytochrome P450 1A1/1A2 in liver and lungs.
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Curcumin decreases 12-O-tetradecanoylphorbol-13-acetate-induced protein kinase C translocation to modulate downstream targets in mouse skin

TL;DR: The results demonstrate the crucial role of PKC in TPA-mediated cellular responses in skin and that curcumin modulates transmembrane signal transduction via PKC to affect Tpa-induced biochemical and molecular alterations in mouse skin.
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Protein Kinase C Epsilon Cooperates with PTEN Loss for Prostate Tumorigenesis through the CXCL13-CXCR5 Pathway.

TL;DR: It is demonstrated that PKCε cooperates with the loss of the tumor suppressor Pten for the development of prostate cancer in a mouse model and identified a compelling rationale for targeting the CXCL13-CXCR5 axis for prostate cancer treatment.
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Activation of Nuclear Factor κB (NF-κB) in Prostate Cancer Is Mediated by Protein Kinase C ϵ (PKCϵ)

TL;DR: In this paper, a strong correlation exists between protein kinase C ϵ (PKCϵ) overexpression and NF-κB activation status in prostate cancer cells, and a mechanistic analysis revealed that TNFα activates PKCϵ via a C1 domain/diacylglycerol-dependent mechanism that involves phosphatidylcholine-phospholipase C.