Rebecca Shaw
· Advanced Practice ClinicianVerifiedUniversity of Utah · Geriatrics
Active 1980–2026
About
Rebecca Shaw is a Nurse Practitioner specializing in Geriatric Psychiatry at the University of Utah Health, primarily practicing at the Madsen Health Center. She holds a Doctor of Nursing Practice (DNP) degree and is recognized for her compassionate, knowledgeable, and patient-centered approach to mental health care. Her extensive experience and dedication are reflected in high patient satisfaction ratings, with many patients describing her as caring, intuitive, and an excellent communicator who listens carefully and includes patients in decision-making about their care. Her clinical focus includes managing medications, addressing issues related to dementia, anxiety, and depression, and providing support for patients and their families through complex health journeys. She is known for her thoroughness, empathy, and ability to create a comfortable environment for her patients, often going above and beyond in follow-up and communication. Her work emphasizes personalized treatment plans, medication management, and holistic support, making her a highly valued provider in her field.
Research topics
- Cell biology
- Biochemistry
- Medicine
- Endocrinology
- Cardiology
- Biology
- Internal medicine
Selected publications
Abstract 4551: Nano-protomers targeted at tumor metastasis
Cancer Research · 2026-04-03
articleAbstract Therapeutic failure in many highly aggressive cancers is often driven by early metastatic spread and poor delivery of effective treatments. Protein-based therapeutics represent an attractive alternative to small-molecule drugs due to their strong biological activity, target selectivity, and generally limited off-target effects. In this work, we investigated whether a HER3-directed fusion construct, HPK, can function as a carrier to transport three different protein payloads—GFP, Gelonin, and GJA1-20k—into HER3-positive tumor cells. By incorporating a simple tagging motif onto each cargo, we assessed HPK’s capacity to load the proteins, recognize HER3 on the tumor cell surface, and promote internal uptake. Our findings show that HPK engages HER3 with high specificity, mediates efficient entry into cancer cells, and delivers intact, functional protein therapeutics. In vivo studies using melanoma and triple-negative breast cancer (TNBC) models further demonstrate that HPK enables payload activity within tumors. Collectively, these results identify HPK as a promising vehicle for successful protein delivery and highlight its potential utility in treating HER3-expressing cancers. Citation Format: Rebecca Benhaghnazar, Dutsin Sirvinas, Joseph Aceves, Ryan Cho, Felix Alonso-Valenteen, Nelyda Gonzalez, Ravinder Abrol, Robin Shaw, Lali Medina-Kauwe. Nano-protomers targeted at tumor metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4551.
bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-16
articleOpen accessABSTRACT Metabolic-associated steatohepatitis (MASH) involves hepatocyte damage that cannot be explained solely by lipid accumulation. Here, to discover injury-specific pathways, we focused on a gene of uncertain function, EF-Hand Domain Family Member D1 (EFHD1), identified in human genome-wide association studies of liver injury but not liver fat. We show that EFHD1, a Ca 2+ -dependent actin crosslinker, stabilizes endoplasmic reticulum–mitochondria contact sites (ERMCS), detecting spatiotemporal coincidence of inter-organellar proximity and ER Ca 2+ release. During MASH, EFHD1 upregulation drives pathological mitochondrial fragmentation via excessive contact persistence. This structural failure promotes mitochondrial double-stranded RNA escape and activation of a maladaptive antiviral PKR-dependent stress response, a causal relationship also supported by Mendelian randomization in humans. Consequently, inhibiting EFHD1 in human and mouse models blunts hepatocyte damage. These findings identify EFHD1 as a Ca 2+ -dependent ERMCS stabilizer, reveal a hepatocyte-intrinsic injury pathway, and suggest EFHD1 inhibition as a therapeutic strategy.
Circulation · 2025-11-03
articleSenior authorBackground: Arrhythmogenic cardiomyopathy (ACM) arises from mutations in desmosomal genes, such as desmoglein (DSG) and desmoplakin (DSP), which converge into a common pathophysiological phenotype at the cellular level, whose hallmarks include disruption of Connexin43 (Cx43) trafficking and membrane localization and suppression of the Wnt/β-catenin signaling pathway. These cellular changes in turn contribute to cardiomyocyte loss, fibrofatty infiltration, and decreased cellular coupling, leading to heart failure, arrhythmias, and sudden cardiac death. GJA1-20k, an internally translated isoform of Cx43, has previously shown therapeutic potential in a DSG model of ACM by preserving Cx43 trafficking and cell-cell coupling. Objective: To investigate the role of GJA1-20k in protecting against a DSP model of ACM by evaluating its effect on Cx43 trafficking and Wnt/β-catenin signaling. Methods: A DSP mutant mouse model of ACM ( Dsp -/- ) received retroorbital injections of AAV9 vectors expressing either GJA1-20k-GFP or GST-GFP at 1×10 12 vg/kg. Echocardiographic measurements were recorded at 4-week intervals until the endpoint was reached, wherein hearts were excised and underwent further processing for histological and biochemical assays. Mechanistic pathways identified were validated in vitro using cell lines. Results: Dsp -/- mice that received GST developed heart failure associated with pathological fibrosis and cardiac remodeling. However, GJA1-20k treated Dsp -/- mice had preserved heart function and absent fibrotic infiltration. At the cardiomyocyte level, GST-treated Dsp -/- mice had significantly reduced Cx43 localization to the intercalated discs and reduced intercalated disc and nuclear localization of β-catenin compared to control mice. This was accompanied by an increase in β-catenin phosphorylation and degradation. However, upon GJA1-20k administration, Dsp -/- mice had restored Cx43 trafficking, increased β-catenin nuclear translocation and activity, and reduced β-catenin degradation. Conclusion: GJA1-20k offers therapeutic potential against ACM by preventing pathological changes in Cx43 localization and Wnt/β-catenin signaling. Moreover, this work introduces the novel concept of next generation gene therapy, whereby targeting common pathological cellular phenotypes downstream of the causative mutation serves as a viable low dose therapeutic approach to diseases of different genetic origin such as ACM.
Design of the First in Human Gene Therapy Trial of TLT-101 for Chronic Heart Failure (FIGHT-HF)
JACC Basic to Translational Science · 2025-02-11 · 4 citations
articleOpen accessSenior authorCorrespondingHeart Rhythm · 2025-04-01
articleOpen accessHeart Rhythm · 2025-04-01
articleCirculation · 2025-11-03
articleIntroduction: Myocardial infarction is a common cause of heart failure (HF), leading to scar tissue formation and increased stress on the cardiac muscle, which affects atrial and ventricular remodeling. We recently showed that gene therapy targeting cardiac bridging integrator 1 (cBIN1) improves left ventricular (LV) function by restoring T-tubule integrity in a canine model of dilated ischemic cardiomyopathy (DICM). However, it is still unclear how this improvement impacts the right ventricular (RV) structural remodeling. Hypothesis: cBIN1 gene therapy delivered intramyocardially in the LV improves RV structural remodeling in a canine model of DICM. Methods: A preclinical canine model of DICM was created by ligating the left anterior descending artery, resulting in a left ventricular ejection fraction < 40% and NT-proBNP level > 900 pmol/L. Ten weeks (±2) post-procedure, dogs were divided into three groups: Group 1 (n=3) received no therapy; Group 2 (n=4) received intramyocardial injections of AAV9 carrying Green Fluorescent Protein (negative control); and Group 3 (n=5) received AAV9-cBIN1. Eight weeks (±2) later, RV mechanical dyssynchrony (septal-free wall peak strain time difference) and RV free wall strain were assessed through echocardiography in awake dogs using a 4-chamber apical view. RV free wall muscle samples were analyzed for T-tubule cross-sectional area using electron microscopy and fibrosis via Masson Trichrome staining. Results: cBIN1-treated animals exhibited significantly improved RV septal-free wall peak strain time difference often refers as septal-to-lateral wall delay - SLWD ( Figure A ) and RV free wall strain - FWS ( Figure B ) compared to the other HF groups that received either the control GFP therapy or no treatment. At both the tissue and subcellular levels, there was a significant improvement in RVFW fibrosis ( Figure C ) and T-tubule cross-sectional area ( Figure D ) in the cBIN1 group compared to the GFP-treated and untreated animals. Furthermore, there were no observable differences between the untreated and GFP-treated HF groups. Conclusions: Reducing mechanical stress across the LV segments through intramyocardial delivery of cBIN1 gene therapy significantly decreased fibrosis in the RVFW muscle by restoring the T-tubule membrane architecture, which in turn improved RV strain and reduced electromechanical dyssynchrony. The study provides preclinical data to mitigate negative remodeling of the RV following ischemic events.
Circulation Heart Failure · 2025-04-21
articleCommunications Medicine · 2025-03-27 · 15 citations
articleOpen accessSenior authorIschemic cardiomyopathy and resultant heart failure (HF) is a significant cause of morbidity and mortality worldwide. Downregulation of cardiac bridging integrator 1 (cBIN1), a membrane scaffolding protein responsible for organizing t-tubules and organizing the calcium handing apparatus, occurs in progressive HF. Therefore, gene therapy upregulating cBIN1 production may rescue failing muscle and clinical HF. Adult mongrel dogs underwent ligation of the left anterior descending artery and developed progressive dilated cardiomyopathy and chronic HF. When left ventricular ejection fraction (LVEF) dropped below 40%, the animals received a one-time series of endocardial injections of either of low dose gene therapy composed of either adeno-associated virus serotype 9 packaged cBIN1 (AAV9-cBIN1, n = 6) or AAV9-GFP (green fluorescent protein, n = 4). Animals were followed up to 7 weeks after therapy delivery with laboratory, echocardiography, and endocardial mapping assessment. Post injection of the negative control, animals develop progressive symptomatic HF requiring early termination of all but one animal prior to the end of the study. In contrast, the AAV9-cBIN1-treated group reveals a significant improvement in LV function, with a noticeable improvement in LVEF (29 ± 3% vs. 42 ± 2%, p = 0.0095) and global longitudinal strain (−7.1 ± 0.9% vs. −12.5 ± 1.6%, p = 0.0095). Compared to the control animals, the AAV9-cBIN1-treated group displays improved T-tubule morphology, left ventricular chamber size, plasma biomarkers, and endocardial voltage, and survives the study period. Chronic HF from ischemic cardiomyopathy can be successfully treated with low dose AAV9-cBIN1 gene therapy. This study indicates that myocardial specific therapy can dramatically reverse HF progression. Blocked heart arteries are known to damage heart muscle by impairing the ability of the heart to pump blood, resulting in progressive muscle damage and eventual heart failure. Medical interventions that recover failing heart muscle are needed to prevent hospitalization or death. Here, we developed a gene therapy to replace an important heart muscle protein, cardiac bridging integrator 1 (cBIN1), and tested it in a canine model of heart failure induced by blocked heart arteries. These findings show improved cardiac muscle function and survival rate following cBIN1 gene therapy, indicating the potential of this gene therapy to reduce the syndrome of heart failure. Khan et al. perform AAV9-cBIN1 gene therapy in a canine model of acquired chronic ischemic cardiomyopathy. They show AAV9-cBIN1 therapy mitigates disease progression and can reverse heart failure in this model.
Heart Rhythm · 2025-04-01
articleOpen access
Recent grants
Regulation of Cav1.2 Trafficking by GJA1-20k and cBIN1
NIH · $2.2M · 2021–2025
NIH · $607k · 2010
NIH · $3.6M · 2019
A New Non-Canonical Role for an Alternatively Translated Ion Channel Protein
NIH · $2.1M · 2017–2022
Unlocking Trafficking Specificity for Cx43 Gap Junctions
NIH · $1.5M · 2020–2025
Frequent coauthors
- 116 shared
TingTing Hong
Second Affiliated Hospital of Zhejiang University
- 36 shared
James W. Smyth
Biomedical Research Institute
- 30 shared
Shaohua Xiao
University of California, Los Angeles
- 29 shared
Rachel Baum
- 28 shared
Lily Yeh Jan
University of California, San Francisco
- 27 shared
André G. Kléber
Beth Israel Deaconess Medical Center
- 26 shared
Sosse Agvanian
Cedars-Sinai Smidt Heart Institute
- 25 shared
Wassim A. Basheer
Cedars-Sinai Smidt Heart Institute
Education
- 1999
M.D. and Ph.D., Biomedical Engineering
Case Western Reserve University
- 1990
Sc.B., Bioelectrical Engineering
Brown University
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