Professor, Medicine, University of Miami School of Medicine
Cardiology
Dr. Nanette H. Bishopric, MD
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Nanette Bishopric works in the field of Cardiology. He graduated from Duke University School of Medicine. Duke University School of Medicine is a top medical college. Duke University School of Medicine is ranked 8 in research and 29 in primary care medicine He over the years received 3 awards: "Member", "Distinguished Scientist Award" and "Fellow (FACC)". Nanette Bishopric is a published doctor and has 86 publications published. The lastest was: 'Modulation of cytokine-induced cardiac myocyte apoptosis by nitric oxide, Bak, and Bcl-x.' He accepts Medicare payments and is registered with Medicare.gov.
Publications
- A cardiac myocyte-restricted Lin28/let-7 regulatory axis promotes hypoxia-mediated apoptosis by inducing the AKT signaling suppressor PIK3IP1.
- Association between anti-human heat shock protein-60 and interleukin-2 with Coronary artery calcium score.
- Dysfunctional potassium channel subunit interaction as a novel mechanism of long QT Syndrome.
- PI3K/mTOR inhibition can impair tumor invasion and metastasis in vivo despite a lack of antiproliferative action in vitro: implications for targeted therapy.
- Toward a genomic definition of aspirin resistance.
- The virtue of just enough stress: a molecular model.
- Auto-acetylation stabilizes p300 in cardiac myocytes during Acute oxidative stress, promoting STAT3 accumulation and cell survival.
- Repression of miR-142 by p300 and MAPK is required for survival signalling via gp130 during adaptive hypertrophy.
- A Large Candidate Gene Survey Identifies the KCNE1 D85N Polymorphism as a Possible Modulator of Drug-Induced Torsades de Pointes.
- Heterogeneity in SDF-1 expression defines the vasculogenic potential of adult cardiac progenitor cells.
- Inflammation, stem cells and atherosclerosis genetics.
- Genome-wide association study identifies a susceptibility locus at 21q21 for ventricular fibrillation in Acute myocardial infarction.
- Comparison of microsomal prostaglandin E synthase-1 deletion and COX-2 inhibition in Acute cardiac ischemia in mice.
- The effects of microsomal prostaglandin E synthase-1 deletion in Acute cardiac ischemia in mice.
- Dilated Cardiomyopathy with increased SR Ca2+ loading preceded by a hypercontractile state and diastolic failure in the alpha(1C)TG mouse.
- Quantitative control of adaptive cardiac hypertrophy by acetyltransferase p300.
- Mesenchymal stem cell-derived IL-10 and recovery from Infarction: a third pitch for the chord.
- Neuroprotective antioxidant STAZN protects against Myocardial ischemia/reperfusion injury.
- Regulation of Bnip3 death pathways by calcium, phosphorylation, and hypoxia-reoxygenation.
- Jun kinase delays caspase-9 activation by interaction with the apoptosome.
- PKC-alpha and TAK-1 are intermediates in the activation of c-Jun NH2-terminal kinase by hypoxia-reoxygenation.
- Whole blood RNA offers a rapid, comprehensive approach to genetic diagnosis of cardiovascular Diseases.
- Redox stress and the contributions of BH3-only proteins to Infarction.
- Acidosis regulates the stability, hydrophobicity, and activity of the BH3-only protein Bnip3.
- Evolution of the Heart from bacteria to man.
- Reversible connexin 43 dephosphorylation during hypoxia and reoxygenation is linked to cellular ATP levels.
- Mitochondrial signals initiate the activation of c-Jun N-terminal kinase (JNK) by hypoxia-reoxygenation.
- Recurrent third-trimester fetal loss and maternal mosaicism for long-QT Syndrome.
- Apoptosis inhibitors for heart Disease.
- Transplantation of stem cells to the Heart:.
- Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3.
- Angiotensin signaling and apoptosis in the neonatal Heart: necessary evils?
- Preventing apoptosis with thioredoxin: ASK me how.
- Bucindolol displays intrinsic sympathomimetic activity in human myocardium.
- MicroRNA-20a Constrains p300-Driven Myocardial Angiogenic Transcription by Direct Targeting of p300.
- Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stress.
- Molecular mechanisms of apoptosis in the cardiac myocyte.
- [Molecular regulation of Myocardial apoptosis].
- Oxidation of zinc finger transcription factors: physiological consequences.
- Reperfusion-activated Akt kinase prevents apoptosis in transgenic mouse Hearts overexpressing insulin-like growth factor-1.
- Molecular regulation of the endothelin-1 gene by hypoxia. Contributions of hypoxia-inducible factor-1, activator protein-1, GATA-2, AND p300/CBP.
- Cytoprotection by Jun kinase during nitric oxide-induced cardiac myocyte apoptosis.
- Control of cardiac-specific transcription by p300 through myocyte enhancer factor-2D.
- Molecular aspects and gene therapy prospects for diastolic Failure.
- Inhibition of p53 function prevents renin-angiotensin system activation and stretch-mediated myocyte apoptosis.
- A glycolytic pathway to apoptosis of hypoxic cardiac myocytes. Molecular pathways of increased acid production.
- Rapid activation of neutral sphingomyelinase by hypoxia-reoxygenation of cardiac myocytes.
- Hypoxia-activated apoptosis of cardiac myocytes requires reoxygenation or a pH shift and is independent of p53.
- Instability of a multiple copy enhancer in plasmid vectors: practical considerations.
- Modulation of cytokine-induced cardiac myocyte apoptosis by nitric oxide, Bak, and Bcl-x.
- Hypoxia regulates beta-enolase and pyruvate kinase-M promoters by modulating Sp1/Sp3 binding to a conserved GC element.
- Angiotensin II receptor subtype AT1 and AT2 expression after Heart transplantation.
- Hypoxia regulates expression of the endothelin-1 gene through a proximal hypoxia-inducible factor-1 binding site on the antisense strand.
- Regulated expression of a foreign gene targeted to the ischaemic myocardium.
- Nonradioactive method for the determination of internucleosomal cleavage associated with apoptosis.
- Adenovirus E1A inhibits cardiac myocyte-specific gene expression through its amino terminus.
- Three-dimensional reconstitution of embryonic cardiomyocytes in a collagen matrix: a new Heart muscle model system.
- Atrial natriuretic peptide induces apoptosis in neonatal rat cardiac myocytes.
- Fusigenic liposome-mediated DNA transfer into cardiac myocytes.
- Cell-specificity and signaling pathway of endothelin-1 gene regulation by hypoxia.
- Expression of inducible nitric oxide synthase in human Heart failure.
- Physical and functional sensitivity of zinc finger transcription factors to redox change.
- Induction and nuclear accumulation of fos and jun proto-oncogenes in hypoxic cardiac myocytes.
- Negative lusitropy and abnormal calcium handling in hypoxic cardiac myocytes exposed to the calcium-sensitizer EMD 53998.
- Regulation of fos and jun immediate-early genes by redox or metabolic stress in cardiac myocytes.
- Cardioprotection in an in vitro model of hypoxic preconditioning.
- Beta adrenergic receptors in lymphocyte subpopulations.
- Dual trophic effects of the alpha 1-adrenergic receptor in cultured neonatal rat Heart muscle cells.
- Cardiac myocyte hypertrophy is associated with c-myc protooncogene expression.
- Induction of the skeletal alpha-actin gene in alpha 1-adrenoceptor-mediated hypertrophy of rat cardiac myocytes.
- Adrenergic regulation of the skeletal alpha-actin gene promoter during Myocardial cell hypertrophy.
- Myocardial activation of the human cardiac alpha-actin promoter by helix-loop-helix proteins.
- Positive regulation of the skeletal alpha-actin gene by Fos and Jun in cardiac myocytes.
- Beta-adrenergic regulation of a Myocardial actin gene via a cyclic AMP-independent pathway.
- Molecular regulation of cardiac myocyte adaptations to Chronic hypoxia.
- Identification of alpha-adrenergic receptors in human platelets by [3H]dihydroergocryptine binding.
- Gene and cell therapy for heart Disease.
- Possible therapeutic targets in cardiac myocyte apoptosis.
- A unique pathway of cardiac myocyte death caused by hypoxia-acidosis.
- A thousand times NO.
- BNip3 and signal-specific programmed death in the Heart.
- Nitric oxide and promotion of cardiac myocyte apoptosis.
- Expression of alpha-synuclein mRNA in Parkinson's Disease.
- Is the G2019S LRRK2 mutation common in all southern European populations?
- Expression of Lewy body protein septin 4 in postmortem brain of Parkinson's Disease and control subjects.
Schools
Duke University School Of Medicine
Duke University Med Center
University Fla
Procedures Preformed
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Imaging
- Cardiac Myocardial Perfusion Imaging
- Cardioverter-Defibrillator or Pacemaker Insertion, Removal or Repair
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Conditions Treated
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Valve Disease
- Arrhythmias (incl. Atrial Fibrillation)
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Doctors Specialties
- Cardiology
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- Amerigroup (Wellpoint)
- AvMed
- Blue Card PPO
- Blue Care HMO
- NetworkBlue
- Cigna HMO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- LocalPlus
- Open Access Plus
- Commercial Insurance Company
- Coventry Health Care
- Employer Group Open Access HMO
- Employer Group PPO
- First Health (Coventry Health Care) PPO
- Medicare Advantage PFFS
- Choice Care PPO
- Preferred PPO
- Select HMO
- Medicaid
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Neighborhood Health Partnership
- Options PPO
- United Healthcare
- Worker's Compensation WC
Awards
- Member
- Distinguished Scientist Award
- Fellow (FACC)
Education
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UCSF -
University of Florida -
Duke University Hospital -
Duke University School of Medicine
Hospital
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University of Miami Hospital
Drug Facts
| NPI NUMBER | 1821025560 | |
| NPPES Provider LastName | BISHOPRIC | |
| NPPES Provider FirstName | NANETTE | |
| NPPES Provider ZIPCode | 331361002 | |
| NPPES Provider State | FL | |
| Specialty Description | Cardiology | |
| Total Claim Count | 198.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1821025560 |
| Last Name Of The Provider | BISHOPRIC |
| First Name Of The Provider | NANETTE |
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