Giulia Baldini
Sourced from institutional research profiles (UAMS TRI or ARA).
Professor
Also affiliated: University of Trieste (1983–2012); Columbia University Irving Medical Center (1999); University of Arkansas Medical Center (2019); ETH Zurich (1988); Whitehead Institute for Biomedical Research (1992–1997); Columbia University (1994–2004)
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Giulia Baldini's research focuses on cellular transport and secretion mechanisms, particularly within adipocytes and insulin-secreting cells. Her work has investigated the role of various proteins, including Syndet, a SNARE protein involved in the insulin-induced translocation of GLUT4 to the cell surface, and rab GTP-binding proteins, such as Rab3 isotypes predominantly expressed in adipocytes. Baldini has also studied the subcellular distribution and function of Rab3A, B, C, and D isoforms in insulin-secreting cells, and explored the stimulation-dependent regulation of pH, volume, and quantal size in secretory vesicles.
Her publications also touch upon broader physiological processes, including the melanocortin pathway and its implications for appetite control, as well as the induction of caveolin during adipogenesis and its association with GLUT4. Baldini's research group leads investigations into these areas, contributing to a deeper understanding of metabolic regulation and cellular communication. She is a highly cited researcher with an h-index of 29 across 63 publications.
Metrics
- h-index: 29
- Publications: 61
- Citations: 6,183
Positions
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Professor publications 2006–2024University of Arkansas for Medical Sciences Institution web page
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
- Constitutive Traffic of Melanocortin-4 Receptor in Neuro2A Cells and Immortalized Hypothalamic Neurons
- Obesity-Linked Variants of Melanocortin-4 Receptor Are Misfolded in the Endoplasmic Reticulum and Can Be Rescued to the Cell Surface by a Chemical Chaperone
- Activating Transcription Factor 6 Limits Intracellular Accumulation of Mutant α1-Antitrypsin Z and Mitochondrial Damage in Hepatoma Cells
- Constitutive Cholesterol-dependent Endocytosis of Melanocortin-4 Receptor (MC4R) Is Essential to Maintain Receptor Responsiveness to α-Melanocyte-stimulating Hormone (α-MSH)
- A Novel Melanocortin-4 Receptor Mutation MC4R-P272L Associated with Severe Obesity Has Increased Propensity To Be Ubiquitinated in the ER in the Face of Correct Folding
Showing 5 of 8 shared publications
- Constitutive Cholesterol-dependent Endocytosis of Melanocortin-4 Receptor (MC4R) Is Essential to Maintain Receptor Responsiveness to α-Melanocyte-stimulating Hormone (α-MSH)
- Temporal cAMP Signaling Selectivity by Natural and Synthetic MC4R Agonists
- Exposure of MC4R to agonist in the endoplasmic reticulum stabilizes an active conformation of the receptor that does not desensitize
- Lipid stress inhibits endocytosis of melanocortin-4 receptor from modified clathrin-enriched sites and impairs receptor desensitization
- Temporal Selectivity of Melanocortin‐4 Receptor Agonist to Modulate Signaling by Increased Intracellular cAMP
Showing 5 of 7 shared publications
- Temporal cAMP Signaling Selectivity by Natural and Synthetic MC4R Agonists
- Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum
- Lipid stress inhibits endocytosis of melanocortin-4 receptor from modified clathrin-enriched sites and impairs receptor desensitization
- Selective Survival of Sim1/MC4R Neurons in Diet-Induced Obesity
- Temporal Selectivity of Melanocortin‐4 Receptor Agonist to Modulate Signaling by Increased Intracellular cAMP
Showing 5 of 6 shared publications
- The melanocortin pathway and control of appetite-progress and therapeutic implications
- Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum
- Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice
- Selective Survival of Sim1/MC4R Neurons in Diet-Induced Obesity
- Liraglutide Counteracts Endoplasmic Reticulum Stress in Palmitate-Treated Hypothalamic Neurons without Restoring Mitochondrial Homeostasis
Showing 5 of 6 shared publications
- Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum
- Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice
- Lipid stress inhibits endocytosis of melanocortin-4 receptor from modified clathrin-enriched sites and impairs receptor desensitization
- Selective Survival of Sim1/MC4R Neurons in Diet-Induced Obesity
- Lipid Stress Alters Cell Distribution, Traffic, and Desensitization Properties of Melanocortin‐4 Receptor, a GPCR Involved in Appetite Control
- Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum
- Selective Survival of Sim1/MC4R Neurons in Diet-Induced Obesity
- 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
- Constitutive Traffic of Melanocortin-4 Receptor in Neuro2A Cells and Immortalized Hypothalamic Neurons
- Obesity-Linked Variants of Melanocortin-4 Receptor Are Misfolded in the Endoplasmic Reticulum and Can Be Rescued to the Cell Surface by a Chemical Chaperone
- Constitutive Cholesterol-dependent Endocytosis of Melanocortin-4 Receptor (MC4R) Is Essential to Maintain Receptor Responsiveness to α-Melanocyte-stimulating Hormone (α-MSH)
- Constitutive Traffic of Melanocortin-4 Receptor in Neuro2A Cells and Immortalized Hypothalamic Neurons
- Activating Transcription Factor 6 Limits Intracellular Accumulation of Mutant α1-Antitrypsin Z and Mitochondrial Damage in Hepatoma Cells
- Constitutive Cholesterol-dependent Endocytosis of Melanocortin-4 Receptor (MC4R) Is Essential to Maintain Receptor Responsiveness to α-Melanocyte-stimulating Hormone (α-MSH)
- Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum
- Injury to hypothalamic Sim1 neurons is a common feature of obesity by exposure to high‐fat diet in male and female mice
- Selective Survival of Sim1/MC4R Neurons in Diet-Induced Obesity
- Temporal cAMP Signaling Selectivity by Natural and Synthetic MC4R Agonists
- Temporal Selectivity of Melanocortin‐4 Receptor Agonist to Modulate Signaling by Increased Intracellular cAMP
- Constitutive Cholesterol-dependent Endocytosis of Melanocortin-4 Receptor (MC4R) Is Essential to Maintain Receptor Responsiveness to α-Melanocyte-stimulating Hormone (α-MSH)
- Palmitate‐induced impairment of melanocortin‐4 receptor
- Constitutive Traffic of Melanocortin-4 Receptor in Neuro2A Cells and Immortalized Hypothalamic Neurons
- Constitutive Cholesterol-dependent Endocytosis of Melanocortin-4 Receptor (MC4R) Is Essential to Maintain Receptor Responsiveness to α-Melanocyte-stimulating Hormone (α-MSH)
- NT5E Mutations That Cause Human Disease Are Associated with Intracellular Mistrafficking of NT5E Protein
- Posttranslational regulation of tissue inhibitor of metalloproteinase-1 by calcium-dependent vesicular exocytosis
- NT5E Mutations That Cause Human Disease Are Associated with Intracellular Mistrafficking of NT5E Protein
- Posttranslational regulation of tissue inhibitor of metalloproteinase-1 by calcium-dependent vesicular exocytosis
- NT5E Mutations That Cause Human Disease Are Associated with Intracellular Mistrafficking of NT5E Protein
- Posttranslational regulation of tissue inhibitor of metalloproteinase-1 by calcium-dependent vesicular exocytosis
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