Giulia Baldini
Sourced from institutional research profiles (UAMS TRI or ARA).
Researcher
Also affiliated: University of Trieste (1983–2012); Board of the Swiss Federal Institutes of Technology (1988); University of Arkansas Medical Center (2006–2019); Schlumberger (Ireland) (2002); Whitehead Institute for Biomedical Research (1992–1997); Arkansas Department of Agriculture (2019); Columbia University (1994–2004)
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Giulia Baldini is a faculty member at the University of Arkansas for Medical Sciences. Her research focuses on the molecular mechanisms underlying neuronal function and cellular stress, with a particular emphasis on the melanocortin 4 receptor (MC4R). Baldini's work investigates the localization and role of MC4R in hypothalamic neurons, contributing to our understanding of appetite regulation and energy balance. She also explores how cellular stress, such as that induced by palmitate treatment, affects neuronal health and function, and how pharmacological interventions like liraglutide may counteract these effects. Her research group also examines ER stress and mitochondrial homeostasis in the context of these cellular processes.
Baldini's scholarly output includes 65 publications with over 6,200 citations, reflecting a highly cited researcher designation. She has collaborated with researchers including Kevin D. Phelan at the University of Arkansas for Fayetteville, and Haven Griffin, Kevin D. Raney, and Randall R Rainwater at the University of Arkansas for Medical Sciences. Her recent work has explored the susceptibility of acute lymphoblastic leukemia cells to microtubule depolymerization and has also touched upon tactile device design for human-robot interaction.
Metrics
- h-index: 29
- Publications: 63
- Citations: 6,139
Selected Publications
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MC4R Localizes at Excitatory Postsynaptic and Peri-Postsynaptic Sites of Hypothalamic Neurons in Primary Culture (2024)
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Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis (2022)
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Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways (2022)
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Selective Survival of Sim1/MC4R Neurons in Diet-Induced Obesity (2020)
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Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum (2020)
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Elevation of the unfolded protein response increases RANKL expression (2020)
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The melanocortin pathway and control of appetite-progress and therapeutic implications (2019)
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Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice (2019)
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Lipid Stress Alters Cell Distribution, Traffic, and Desensitization Properties of Melanocortin‐4 Receptor, a GPCR Involved in Appetite Control (2017)
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Lipid stress inhibits endocytosis of melanocortin-4 receptor from modified clathrin-enriched sites and impairs receptor desensitization (2017)
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Indicators of responsiveness to immune checkpoint inhibitors (2017)
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Temporal Selectivity of Melanocortin‐4 Receptor Agonist to Modulate Signaling by Increased Intracellular cAMP (2015)
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Temporal cAMP Signaling Selectivity by Natural and Synthetic MC4R Agonists (2015)
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Does Super-Resolution Fluorescence Microscopy Obsolete Previous Microscopic Approaches to Protein Co-localization? (2014)
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NT5E Mutations That Cause Human Disease Are Associated with Intracellular Mistrafficking of NT5E Protein (2014)
Grants & Funding
As listed on this researcher's institutional profile.
- Super-Resolution Light Microscope at University of Arkansas for Medical Sciences NIH
- Mechanisms of Hormonal Release by Endocrine Cells NIH
- Functions and Mechanisms of Helicases and G-Quadruplex Nucleic Acids NIH
- Impact of hemodynamics on efferocytosis in endothelial cells NIH/Nat. Heart, Lung & Blood Institute
- Lipid Stress and MC4R NIH
- G-quadruplex DNA as a chemical signaling agent NIH
- 120 kV FEI Electron Microscope and Supporting Sample Preparation Equipment for Biological Microscopy National Science Foundation
- Melanocortin-4 Receptor Traffic and Signaling NIH
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences
- Baldini Start up Account UAMS College of Medicine
Collaboration Network
Top Collaborators
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
- MC4R Localizes at Excitatory Postsynaptic and Peri-Postsynaptic Sites of Hypothalamic Neurons in Primary Culture
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
- MC4R Localizes at Excitatory Postsynaptic and Peri-Postsynaptic Sites of Hypothalamic Neurons in Primary Culture
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Primary acute lymphoblastic leukemia cells are susceptible to microtubule depolymerization in G1 and M phases through distinct cell death pathways
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
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