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Department of Biomedical Sciences

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The mission of the Department of Biomedical Sciences is to be "a community of scholars who educate future physicians and scientists and who advance knowledge through discovery. " As a diverse basic science department, we provide a broad foundation for an integrated medical education in the first 2 years of medical school before the students begin their clinical practices. In addition to the role that the Department of Biomedical Sciences plays in education of medical students, we offer a Ph.D. in Biomedical Sciences that trains scientists in contemporary approaches to address questions of developmental, cell, and molecular biology related to human health and an M.S. program that serves as a Bridge to the M.D. Our faculty also participates in 2 interdisciplinary graduate programs on FSU campus: Program in Neuroscience and Molecular Biophysics Graduate Program.

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3'-UTR and microRNA-24 regulate circadian rhythms by repressing PERIOD2 protein accumulation.
3'-UTR and microRNA-24 regulate circadian rhythms by repressing PERIOD2 protein accumulation.
14-3-3 Proteins in Glutamatergic Synapses.
14-3-3 Proteins in Glutamatergic Synapses.
14-3-3 and aggresome formation
14-3-3 and aggresome formation
14-3-3 protein targets misfolded chaperone-associated proteins to aggresomes.
14-3-3 protein targets misfolded chaperone-associated proteins to aggresomes.
14-3-3 proteins are required for hippocampal long-term potentiation and associative learning and memory.
14-3-3 proteins are required for hippocampal long-term potentiation and associative learning and memory.
14-3-3 proteins in neurological disorders.
14-3-3 proteins in neurological disorders.
14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.
14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.
Absence Of Specific Yeast Heat-shock Proteins Leads To Abnormal Aggregation And Compromised Autophagic Clearance Of Mutant Huntingtin Proteins
Absence Of Specific Yeast Heat-shock Proteins Leads To Abnormal Aggregation And Compromised Autophagic Clearance Of Mutant Huntingtin Proteins
Absence of Myocardial Thyroid Hormone Inactivating Deiodinase Results in Restrictive Cardiomyopathy in Mice
Absence of Myocardial Thyroid Hormone Inactivating Deiodinase Results in Restrictive Cardiomyopathy in Mice
Accelerated healing in NONcNZO10/LtJ type 2 diabetic mice by FGF 1
Accelerated healing in NONcNZO10/LtJ type 2 diabetic mice by FGF 1
Activation Profiles of Human Kallikrein-Related Peptidases by Matrix Metalloproteinases
Activation Profiles of Human Kallikrein-Related Peptidases by Matrix Metalloproteinases
Activation Profiles of Human Kallikrein-Related Peptidases by Proteases of the Thrombostasis Axis
Activation Profiles of Human Kallikrein-Related Peptidases by Proteases of the Thrombostasis Axis
Acupoint Sensitization, Acupuncture Analgesia, Acupuncture on Visceral Functional Disorders, and Its Mechanism.
Acupoint Sensitization, Acupuncture Analgesia, Acupuncture on Visceral Functional Disorders, and Its Mechanism.
Acute BDNF treatment upregulates GluR1-SAP97 and GluR2-GRIP1 interactions
Acute BDNF treatment upregulates GluR1-SAP97 and GluR2-GRIP1 interactions
Akt mediated phosphorylation of LARP6; critical step in biosynthesis of type I collagen
Akt mediated phosphorylation of LARP6; critical step in biosynthesis of type I collagen
Akt mediated phosphorylation of LARP6; critical step in biosynthesis of type I collagen.
Akt mediated phosphorylation of LARP6; critical step in biosynthesis of type I collagen.
Allosteric Transmission along a Loosely Structured Backbone Allows a Cardiac Troponin C Mutant to Function with Only One Ca Ion.
Allosteric Transmission along a Loosely Structured Backbone Allows a Cardiac Troponin C Mutant to Function with Only One Ca Ion.
Alternative Folding Nuclei Definitions Facilitate the Evolution of a Symmetric Protein Fold from a Smaller Peptide Motif
Alternative Folding Nuclei Definitions Facilitate the Evolution of a Symmetric Protein Fold from a Smaller Peptide Motif
Amide Hydrogens Reveal A Temperature-dependent Structural Transition That Enhances Site-ii Ca2+ -binding Affinity In A C-domain Mutant Of Cardiac Troponin C
Amide Hydrogens Reveal A Temperature-dependent Structural Transition That Enhances Site-ii Ca2+ -binding Affinity In A C-domain Mutant Of Cardiac Troponin C
Amide hydrogens reveal a temperature-dependent structural transition that enhances site-II Ca(2+)-binding affinity in a C-domain mutant of cardiac troponin C.
Amide hydrogens reveal a temperature-dependent structural transition that enhances site-II Ca(2+)-binding affinity in a C-domain mutant of cardiac troponin C.

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