Crystal R. Archer Data-verified
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Assistant Professor of Biochemistry
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Biography and Research Information
OverviewAI-generated summary
Crystal R. Archer, Assistant Professor of Biochemistry at the University of Arkansas at Fayetteville, investigates the molecular mechanisms regulating ion channel function. Her research group focuses on the epithelial sodium channel (ENaC) and voltage-gated potassium channels (Kv channels), particularly Kv7.2.
Recent work by Archer and her collaborators has explored the roles of casein kinase II, ankyrin-3, and the P2Y2 receptor in modulating ENaC activity. Her team has also investigated the signaling pathways involved in angiotensin II activation of ENaC, including the involvement of NOXA1-dependent NADPH oxidase 1. Furthermore, her research has examined optogenetic control of phosphatidylinositol 4,5-bisphosphate (PIP2) interactions, which are critical for shaping ENaC activity, and the stimulation of ENaC in renal principal cells using designer receptors. Archer also leads a research group that utilizes isothermal titration calorimetry for fragment-based analysis of ion channel interactions.
Archer is the Principal Investigator on a $249,000 grant from the NIH/National Institute of General Medical Sciences. This award supports research into the structural consequences of PKC-dependent phosphorylation of Kv7.2. Her scholarly output includes 33 publications with 490 citations and an h-index of 8. She has one shared publication with collaborator Phuc Phan.
Metrics
- h-index: 8
- Publications: 35
- Citations: 495
Selected Publications
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BPS2026 – Regulation of the KCNQ4 channel via the interplay between phosphorylation, calmodulin, and PIP2 (2026)
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Abstract 2279 Phosphorylation control of Kv7.2 structure and interactions in response to GPCR signals (2025)
Federal Grants 1 $249,000 total
Structural consequences of PKC-dependent phosphorylation of Kv7.2
Collaboration Network
Top Collaborators
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- P2Y2 receptor decreases blood pressure by inhibiting ENaC
- Optogenetic Control of PIP2 Interactions Shaping ENaC Activity
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel
- Stimulation of the Epithelial Na+ Channel in Renal Principal Cells by Gs-Coupled Designer Receptors Exclusively Activated by Designer Drugs
Showing 5 of 8 shared publications
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- P2Y2 receptor decreases blood pressure by inhibiting ENaC
- Optogenetic Control of PIP2 Interactions Shaping ENaC Activity
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel
- Stimulation of the Epithelial Na+ Channel in Renal Principal Cells by Gs-Coupled Designer Receptors Exclusively Activated by Designer Drugs
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- Optogenetic Control of PIP2 Interactions Shaping ENaC Activity
- Functional assessment of PIP <sub>2</sub> regulation of ENaC using an optogenetic dimerization assay
- Abstract MP20: Optogenetic Control Of Pip2 To Assess Mechanisms Regulating The Epithelial Sodium Channel
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- P2Y2 receptor decreases blood pressure by inhibiting ENaC
- Stimulation of the Epithelial Na+ Channel in Renal Principal Cells by Gs-Coupled Designer Receptors Exclusively Activated by Designer Drugs
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel
- Stimulation of the Epithelial Na+ Channel in Renal Principal Cells by Gs-Coupled Designer Receptors Exclusively Activated by Designer Drugs
- P2Y2 receptor decreases blood pressure by inhibiting ENaC
- Stimulation of the Epithelial Na+ Channel in Renal Principal Cells by Gs-Coupled Designer Receptors Exclusively Activated by Designer Drugs
- Optogenetic Control of PIP2 Interactions Shaping ENaC Activity
- TRPM7 Mg2+-permeable channels are prime targets against highly aggressive B cell leukemias
- Abstract 1429: The interplay of casein kinase II and ankyrin G with the key renal ion channel, ENaC, in controlling blood pressure
- Abstract 2135: Structural Impacts of Phosphorylation of the KCNQ2 B Helix on CaM and PIP2 Binding
- P2Y2 receptor decreases blood pressure by inhibiting ENaC
- Cellular and Molecular Mechanisms Regulating the Normal Physiological Function of ENaC in Salt-Sensitive Hypertension
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel
- Stimulation of the Epithelial Na+ Channel in Renal Principal Cells by Gs-Coupled Designer Receptors Exclusively Activated by Designer Drugs
- Abstract MP20: Optogenetic Control Of Pip2 To Assess Mechanisms Regulating The Epithelial Sodium Channel
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel
- NOXA1-dependent NADPH oxidase 1 signaling mediates angiotensin II activation of the epithelial sodium channel
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