Catera Wilder, PhD

Assistant Professor
Department of Bioengineering and Therapeutic Sciences
Wilder.
[email protected]
Phone: +1 415 476-6452
513 Parnassus Avenue, HSE, Rm 1145D
San Francisco, CA 94143
United States

Links

Wilder Lab UCSF Profiles

What I do

I am a biomedical engineer and systems biologist who combines my understanding of signaling system networks in innate immunity with my expertise in molecular biology and tissue remodeling to address pressing questions about immunity and immunopathogenesis.

Departmental research area

therapeutic bioengineering

My research expertise

interferon antiviral response, JAK-STAT/IRF signaling dynamics, inflammatory response, systems biology, mathematical modeling, gene regulatory mechanisms

Professional background

Degrees

PhD, Biomedical Engineering, Georgia Institute of Technology, and Emory University, 2016
BS, Biological Engineering, Music Minor, University of Missouri Columbia, 2009

Postgraduate training

Postdoctoral Training, Signaling Systems Biology, University of California, Los Angeles, 2022

Biography

Catera Wilder, Ph.D. is an Assistant Professor in the Department of Bioengineering and Therapeutic Sciences at the University of California San Francisco and Chan Zuckerberg Biohub Investigator. She received her Ph.D. in Biomedical Engineering at Georgia Institute of Technology and Emory University (2016) under the direction of Manu Platt. As a UCLA Chancellor’s Postdoctoral Fellow in the lab of Alexander Hoffmann (2016-2022) she focused on understanding innate immune and inflammatory responses by studying ISGF3 transcription factor dynamic regulation using a systems biology approach. Her work investigating the interferon signaling and transcriptional regulation has uncovered stimulus specific responses determined by coordinated stimulus-contingent positive feedback loops.

Dr. Wilder devoted much of her training in complementary research areas to develop her own distinctive research program. As a graduate student, her studies showed that perturbations within a proteolytic network using protease inhibitors can upregulate matrix degradation in a cellular localization dependent manner, potentially leading to increased cancer cell invasion or metastasis. She published most of this work in The International Journal of Biochemistry & Cell Biology. During her training, she was awarded the National Science Foundation Graduate Research Fellowship and Ford Foundation Predoctoral Fellowship. Due to collaborations on other projects, she was also a co-author on five other peer reviewed journal articles.

Her passion to understand the complexity of cellular responses led her to study cellular signaling networks in innate immunity as a postdoctoral fellow. From these studies, she demonstrated distinct regulation of antiviral and inflammatory gene expression programs by different interferon cytokines control of feedback and feedforward loops. One manuscript for this work is currently in preparation and another published in Frontiers in Immunology. She was the recipient of the UCLA Chancellor’s Postdoctoral Fellowship award and two NIH T32 Postdoctoral Fellowship awards.

Research keywords

  • Interferon-Stimulated Gene Factor 3
  • Academic Success
  • STAT1 Transcription Factor
  • Cathepsin L
  • transcription factors
  • Cathepsins
  • Feedback
  • Cathepsin K
  • biochemistry
  • Protease Inhibitors
  • Schools
  • Leucine
  • Feedback, Physiological
  • Gene Expression Regulation
  • Cystatin C

Publications

Luecke S, Schiffman A, Singh A, Huang H, Shannon B, Wilder CL. Four guiding principles for effective trainee-led STEM community engagement through high school outreach. PLoS Comput Biol. 2023 05; 19(5):e1011072.
Wilder CL, Lefaudeux D, Mathenge R, Kishimoto K, Zuniga Munoz A, Nguyen MA, Meyer AS, Cheng QJ, Hoffmann A. A stimulus-contingent positive feedback loop enables IFN-β dose-dependent activation of pro-inflammatory genes. Mol Syst Biol. 2023 05 09; 19(5):e11294.
Kishimoto K, Wilder CL, Buchanan J, Nguyen M, Okeke C, Hoffmann A, Cheng QJ. High Dose IFN-β Activates GAF to Enhance Expression of ISGF3 Target Genes in MLE12 Epithelial Cells. Front Immunol. 2021; 12:651254.
Shockey WA, Kieslich CA, Wilder CL, Watson V, Platt MO. Dynamic Model of Protease State and Inhibitor Trafficking to Predict Protease Activity in Breast Cancer Cells. Cell Mol Bioeng. 2019 Aug; 12(4):275-288.
Wilder CL, Walton C, Watson V, Stewart FAA, Johnson J, Peyton SR, Payne CK, Odero-Marah V, Platt MO. Differential cathepsin responses to inhibitor-induced feedback: E-64 and cystatin C elevate active cathepsin S and suppress active cathepsin L in breast cancer cells. Int J Biochem Cell Biol. 2016 10; 79:199-208.
Porter KM, Wieser FA, Wilder CL, Sidell N, Platt MO. Cathepsin Protease Inhibition Reduces Endometriosis Lesion Establishment. Reprod Sci. 2016 May; 23(5):623-9.
Burton LJ, Smith BA, Smith BN, Loyd Q, Nagappan P, McKeithen D, Wilder CL, Platt MO, Hudson T, Odero-Marah VA. Muscadine grape skin extract can antagonize Snail-cathepsin L-mediated invasion, migration and osteoclastogenesis in prostate and breast cancer cells. Carcinogenesis. 2015 Sep; 36(9):1019-27.
Keegan PM, Wilder CL, Platt MO. Tumor necrosis factor alpha stimulates cathepsin K and V activity via juxtacrine monocyte-endothelial cell signaling and JNK activation. Mol Cell Biochem. 2012 Aug; 367(1-2):65-72.
Wilder CL, Park KY, Keegan PM, Platt MO. Manipulating substrate and pH in zymography protocols selectively distinguishes cathepsins K, L, S, and V activity in cells and tissues. Arch Biochem Biophys. 2011 Dec 01; 516(1):52-7.
Li WA, Barry ZT, Cohen JD, Wilder CL, Deeds RJ, Keegan PM, Platt MO. Detection of femtomole quantities of mature cathepsin K with zymography. Anal Biochem. 2010 Jun 01; 401(1):91-8.
Platt MO, Wilder CL, Wells A, Griffith LG, Lauffenburger DA. Multipathway kinase signatures of multipotent stromal cells are predictive for osteogenic differentiation: tissue-specific stem cells. Stem Cells. 2009 Nov; 27(11):2804-14.