Professor, Biochemistry and Biophysics, Perelman School of Medicine
Internal Medicine
Dr. Roland G. Kallen, MD
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Dr. Roland G. Kallen practices Internal Medicine. He studied medicine at Columbia University College of Physicians & Surgeons. Columbia University College of Physicians & Surgeons is one of the top medical schools in the US. Columbia University College of Physicians & Surgeons is ranked 8/52 in Research/PrimaryCare. Doctor Roland G. Kallen, MD is a published physician. He has 52 publications published. The most current publication "Extrapore residues of the S5-S6 loop of domain 2 of the voltage-gated skeletal muscle sodium channel (rSkM1) contribute to the mu-conotoxin GIIIA binding site."
Publications
- Studies of alpha-helicity and intersegmental interactions in voltage-gated Na+ channels: S2D4.
- Direct Evidence that Scorpion α-Toxins (Site-3) Modulate Sodium Channel Inactivation by Hindrance of Voltage-Sensor Movements.
- Sea anemone toxin (ATX II) modulation of heart and skeletal muscle sodium channel alpha-subunits expressed in tsA201 cells.
- Analysis of a T4 DNA replication protein complex. Studies of the DNA recognition site for T4 gene 44/62 and 45 protein-catalyzed ATP hydrolysis.
- Differences in the binding sites of two site-3 sodium channel toxins.
- A strategy for generating monoclonal antibodies against recombinant baculovirus-produced proteins: application to the Bcl-2 oncoprotein.
- TTX-sensitive and TTX-insensitive sodium channel mRNA transcripts are independently regulated in adult skeletal muscle after denervation.
- Synthesis, purification, and characterization of the cytoplasmic domain of the human insulin receptor using a baculovirus expression system.
- Assignment of a human skeletal muscle sodium channel alpha-subunit gene (SCN4A) to 17q23.1-25.3.
- Expression and characterization of the rat D3 dopamine receptor: pharmacologic properties and development of antibodies.
- Pharmacological modulation of human cardiac Na+ channels.
- A molecular link between activation and inactivation of sodium channels.
- Modulation of human muscle sodium channels by intracellular fatty acids is dependent on the channel isoform.
- RFLP for BglII at the human skeletal muscle sodium channel locus.
- Interaction between the skeletal muscle type 1 Na+ channel promoter E-box and an upstream repressor element. Release of repression by myogenin.
- Chimeric study of sodium channels from rat skeletal and cardiac muscle.
- Restoration of fast inactivation in an inactivation-defective human heart sodium channel by the cysteine modifying reagent benzyl-MTS: analysis of IFM-ICM mutation.
- Modulation of the human cardiac sodium channel alpha-subunit by cAMP-dependent protein kinase and the responsible sequence domain.
- Identification of a mutation in the gene causing hyperkalemic periodic paralysis.
- Electrophysiological characteristics of cloned skeletal and cardiac muscle sodium channels.
- Two E-boxes are the focal point of muscle-specific skeletal muscle type 1 Na+ channel gene expression.
- Differences in steady-state inactivation between Na channel isoforms affect local anesthetic binding affinity.
- Expressed Na channel clones differ in their sensitivity to external calcium concentration.
- Effects of tyrosine-->phenylalanine mutations on auto- and trans-phosphorylation reactions catalyzed by the insulin receptor beta-subunit cytoplasmic domain.
- Stable expression and functional characterization of a human cardiac Na+ channel gene in mammalian cells.
- Genomic organization of the human skeletal muscle sodium channel gene.
- Evidence for a direct interaction between internal tetra-alkylammonium cations and the inactivation gate of cardiac sodium channels.
- Pore residues critical for mu-CTX binding to rat skeletal muscle Na+ channels revealed by cysteine mutagenesis.
- The Na channel voltage sensor associated with inactivation is localized to the external charged residues of domain IV, S4.
- Functional consequences of sulfhydryl modification in the pore-forming subunits of cardiovascular Ca2+ and Na+ channels.
- Beta-adrenergic modulation of currents produced by rat cardiac Na+ channels expressed in Xenopus laevis oocytes.
- Primary structure of the adult human skeletal muscle voltage-dependent sodium channel.
- On the molecular nature of the lidocaine receptor of cardiac Na+ channels. Modification of block by alterations in the alpha-subunit III-IV interdomain.
- SkM2, a Na+ channel cDNA clone from denervated skeletal muscle, encodes a tetrodotoxin-insensitive Na+ channel.
- Extrapore residues of the S5-S6 loop of domain 2 of the voltage-gated skeletal muscle sodium channel (rSkM1) contribute to the mu-conotoxin GIIIA binding site.
- Primary structure and expression of a sodium channel characteristic of denervated and immature rat skeletal muscle.
- Lidocaine block of human heart sodium channels expressed in Xenopus oocytes.
- Primary structure and functional expression of a mammalian skeletal muscle sodium channel.
- Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel.
- Characterizing the mu-conotoxin binding site on voltage-sensitive sodium channels with toxin analogs and channel mutations.
- Glutamine substitution at alanine1649 in the S4-S5 cytoplasmic loop of domain 4 removes the voltage sensitivity of fast inactivation in the human heart sodium channel.
- Nomenclature of voltage-gated sodium channels.
- Effects of Tityus serrulatus scorpion toxin gamma on voltage-gated Na+ channels.
- Molecular cloning and functional analysis of the promoter of rat skeletal muscle voltage-sensitive sodium channel subtype 2 (rSkM2): evidence for muscle-specific nucle...
- Structure, function and expression of voltage-dependent sodium channels.
- Dual tandem promoter elements containing CCAC-like motifs from the tetrodotoxin-resistant voltage-sensitive Na+ channel (rSkM2) gene can independently drive muscle-spe...
- A unique role for the S4 segment of domain 4 in the inactivation of sodium channels.
- A carboxy-terminal alpha-helical segment in the rat skeletal muscle voltage-dependent Na+ channel is responsible for its interaction with the amino-terminus.
- An ''Old World'' scorpion beta-toxin that recognizes both insect and mammalian sodium channels.
- Lidocaine stabilizes the open state of CNS voltage-dependent sodium channels.
- Location analysis for the estrogen receptor-alpha reveals binding to diverse ERE sequences and widespread binding within repetitive DNA elements.
Schools
Columbia University College of Physicians And Surgeons
Doctors Specialties
- Cardiology
- Hematology
- Internal Medicine
Accepted Insurances
Education
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NYU School of Medicine -
Columbia University College of Physicians & Surgeons
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