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Cindy K. Miranti

Researcher at University of Arizona

Publications -  68
Citations -  8720

Cindy K. Miranti is an academic researcher from University of Arizona. The author has contributed to research in topics: Prostate cancer & Integrin. The author has an hindex of 28, co-authored 65 publications receiving 7530 citations. Previous affiliations of Cindy K. Miranti include Roosevelt Institute & Jewish Hospital.

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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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Sensing the environment: a historical perspective on integrin signal transduction.

TL;DR: This historical perspective traces the key findings that have led to the current understanding of these important functions of integrins.
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Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

TL;DR: It is demonstrated that the transcription factors serum response factor (SRF) and Elk-1 can mediate glutamate induction of transcription through the SRE in cortical neurons, suggesting that SRF, Elk, and ERKs may have important roles in neuroplasticity.
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A growth factor-induced kinase phosphorylates the serum response factor at a site that regulates its DNA-binding activity.

TL;DR: A model in which the growth factor-induced phosphorylation of SRF contributes to the activation of c-fos transcription by facilitating the formation of an active transcription complex at the serum response element is suggested.
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Calcium activates serum response factor-dependent transcription by a Ras- and Elk-1-independent mechanism that involves a Ca2+/calmodulin-dependent kinase

TL;DR: Findings indicate that SRF is a versatile transcription factor that, when bound to the SRE, can function by distinct mechanisms and can mediate transcriptional responses to both CaMK- and Ras-dependent signaling pathways.