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Vijayasaradhi Setaluri

Researcher at University of Wisconsin-Madison

Publications -  68
Citations -  7426

Vijayasaradhi Setaluri is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Melanoma & Microphthalmia-associated transcription factor. The author has an hindex of 28, co-authored 62 publications receiving 6171 citations. Previous affiliations of Vijayasaradhi Setaluri include Veterans Health Administration.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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MAGE-A, mMage-b, and MAGE-C Proteins Form Complexes with KAP1 and Suppress p53-Dependent Apoptosis in MAGE-Positive Cell Lines

TL;DR: In this paper, the authors showed that MAGE-specific small interfering RNA suppresses S91 melanoma growth in vivo, in syngenic DBA2 mice and showed that suppression of class I MAGE proteins induces apoptosis in the Hs-294T, A375, and S91 MAGE positive melanoma cell lines and that members of all three families of MAGE class I proteins form complexes with KAP1, a scaffolding protein known as a corepressor of p53 expression and function.
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Aberrant retention of tyrosinase in the endoplasmic reticulum mediates accelerated degradation of the enzyme and contributes to the dedifferentiated phenotype of amelanotic melanoma cells

TL;DR: In this paper, the authors investigated whether the loss of tyrosinase was due to proteolytic degradation, and they found that the degradation process was more prominent in malignant than in normal melanocytes and promoted the maturation and transit from the ER to the Golgi compartment.
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Microtubule-associated proteins as targets in cancer chemotherapy.

TL;DR: It is proposed that rational microtubule-targeting cancer therapeutic approaches should ideally include proteomic profiling of tumor MAPs before administration of micro Tubule-stabilizing/destabilizing agents preferentially in combination with agents that modulate the expression of relevant MAPs.