Professor, Medicine, Case Western Reserve University School of Medicine
Hematology
Dr. Clark W. Distelhorst, MD
|
|
Give Review
Clark W. Distelhorst practices Hematology. He went to The Ohio State University College of Medicine. He has 1 awards "Elected Member". Clark W. Distelhorst has written publications. He has 84 publications published with PubMed. The lastest publication is: 'c-Fos degradation by the proteasome. An early, Bcl-2-regulated step in apoptosis.' He is registered with Medicare.
Publications
- Feedback regulation mediated by Bcl-2 and DARPP-32 regulates inositol 1,4,5-trisphosphate receptor phosphorylation and promotes Cell survival.
- Acidosis blocks CCAAT/enhancer-binding protein homologous protein (CHOP)- and c-Jun-mediated induction of p53-upregulated mediator of apoptosis (PUMA) during amino aci...
- Glucocorticoid elevation of dexamethasone-induced gene 2 (Dig2/RTP801/REDD1) mediates autophagy in lymphocytes.
- Bcl-2 interaction with the inositol 1,4,5-trisphosphate receptor: Role in Ca(2+) signaling and Disease.
- Induction of Ca²+-driven apoptosis in Chronic lymphocytic leukemia cells by peptide-mediated disruption of Bcl-2-IP3 receptor interaction.
- Glucocorticoid-mediated repression of the oncogenic microRNA cluster miR-17~92 contributes to the induction of Bim and initiation of apoptosis.
- Glucocorticoids downregulate Fyn and inhibit IP(3)-mediated calcium signaling to promote autophagy in T lymphocytes.
- Apoptosis and autophagy: decoding calcium signals that mediate life or death.
- Glucocorticoid-mediated inhibition of Lck modulates the pattern of T Cell receptor-induced calcium signals by down-regulating inositol 1,4,5-trisphosphate receptors.
- The BH4 domain of Bcl-2 inhibits ER calcium release and apoptosis by binding the regulatory and coupling domain of the IP3 receptor.
- Targeting Bcl-2-IP3 receptor interaction to reverse Bcl-2's inhibition of apoptotic calcium signals.
- Apoptosis inhibition by Bcl-2 gives way to autophagy in glucocorticoid-treated lymphocytes.
- Dexamethasone-induced inositol 1,4,5-trisphosphate receptor elevation in murine Lymphoma cells is not required for dexamethasone-mediated calcium elevation and apoptosis.
- Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes.
- Bcl-2 protein family members: versatile regulators of calcium signaling in Cell survival and apoptosis.
- Bcl-2-regulated calcium signals as common mediators of both apoptosis and autophagy.
- Live free or die: an immature T Cell decision encoded in distinct Bcl-2 sensitive and insensitive Ca2+ signals.
- Bcl-2 differentially regulates Ca2+ signals according to the strength of T Cell receptor activation.
- The glucocorticoid-induced gene tdag8 encodes a pro-apoptotic G protein-coupled receptor whose activation promotes glucocorticoid-induced apoptosis.
- Bcl-2 functionally interacts with inositol 1,4,5-trisphosphate receptors to regulate calcium release from the ER in response to inositol 1,4,5-trisphosphate.
- Dexamethasone-induced gene 2 (dig2) is a novel pro-survival stress gene induced rapidly by diverse apoptotic signals.
- Microarray analysis uncovers the induction of the proapoptotic BH3-only protein Bim in multiple models of glucocorticoid-induced apoptosis.
- Bcl-2 on the endoplasmic reticulum regulates Bax activity by binding to BH3-only proteins.
- Lyn Facilitates Glioblastoma Cell Survival under Conditions of Nutrient Deprivation by Promoting Autophagy.
- Bcl-2 suppresses Ca2+ release through inositol 1,4,5-trisphosphate receptors and inhibits Ca2+ uptake by mitochondria without affecting ER calcium store content.
- Targeting Bcl-2 based on the interaction of its BH4 domain with the inositol 1,4,5-trisphosphate receptor.
- The Cellular concentration of Bcl-2 determines its pro- or anti-apoptotic effect.
- Cell biology. Apoptosis--the calcium connection.
- Bcl-2 and calcium: controversy beneath the surface.
- Bcl-2 on the endoplasmic reticulum: protecting the mitochondria from a distance.
- Recent insights into the mechanism of glucocorticosteroid-induced apoptosis.
- Transient expression of wild-type or mitochondrially targeted Bcl-2 induces apoptosis, whereas transient expression of endoplasmic reticulum-targeted Bcl-2 is protecti...
- Unreliability of the cytochrome c-enhanced green fluorescent fusion protein as a marker of cytochrome c release in Cells that overexpress Bcl-2.
- Involvement of c-Fos in signaling grp78 induction following ER calcium release.
- c-Fos degradation by the proteasome. An early, Bcl-2-regulated step in apoptosis.
- Apoptosis induction by the glucocorticoid hormone dexamethasone and the calcium-ATPase inhibitor thapsigargin involves Bc1-2 regulated caspase activation.
- Regulation of Bcl-xl channel activity by calcium.
- Fas-induced proteolytic activation and intraCellular redistribution of the stress-signaling kinase MEKK1.
- Role of calcium in glucocorticosteroid-induced apoptosis of thymocytes and Lymphoma cells: resurrection of old theories by new findings.
- Bcl-2 inhibits c-fos induction by calcium.
- Maintenance of calcium homeostasis in the endoplasmic reticulum by Bcl-2.
- Baculovirus p35 and Z-VAD-fmk inhibit thapsigargin-induced apoptosis of Breast cancer cells.
- Glucocorticoid-induced apoptosis.
- Mouse Lymphoma cells destined to undergo apoptosis in response to thapsigargin treatment fail to generate a calcium-mediated grp78/grp94 stress response.
- Bcl-2 acts subsequent to and independent of Ca2+ fluxes to inhibit apoptosis in thapsigargin- and glucocorticoid-treated mouse Lymphoma cells.
- Bcl-2 inhibits hydrogen peroxide-induced ER Ca2+ pool depletion.
- Steroid hormone receptors.
- Relationship between defective mouse mammary tumor virus envelope glycoprotein synthesis and GRP78 synthesis in glucocorticoid-treated mouse Lymphoma cells. Evidence f...
- Effect of glucocorticosteroid treatment on intracellular calcium homeostasis in mouse Lymphoma cells.
- Evidence that BCL-2 represses apoptosis by regulating endoplasmic reticulum-associated Ca2+ fluxes.
- Autosomal Dominant familial erythrocytosis due to autonomous erythropoietin production.
- Glucocorticoid receptor content of T lymphocytes: evidence for heterogeneity.
- Effect of mitogen concentration on glucocorticoid suppression of normal and cystic fibrosis lymphocyte activation.
- Effect of mitogenic and high, nonmitogenic concentrations of phytohemagglutinin and concanavalin A on the number of human lymphocytes in culture.
- Effect of Cell cycle position on dexamethasone binding by mouse and human lymphoid Cell lines: correlation between an increase in dexamethasone binding during S phase ...
- Centrifugal elutriation of human lymphoid Cells: synchronization and separation of aneuploid Cells into diploid and tetraploid populations.
- Activation of the rat Liver cytosol glucocorticoid receptor by sephacryl S-300 filtration in the presence and absence of molybdate. Physical properties of the receptor...
- A single common electrophoretic abnormality of glucocorticoid receptors in human Leukemia cells.
- Characterization of glucocorticoid receptors in S49 mouse Lymphoma cells by affinity labeling with [3H]dexamethasone 21-mesylate.
- Immunochemical comparison of mutant glucocorticoid receptors and wild type receptor fragments produced by neutrophil elastase and chymotrypsin.
- Characterization of glucocorticoid receptors and glucocorticoid receptor mRNA in human Leukemia cells: stabilization of the receptor by diisopropylfluorophosphate.
- Effect of the 90 kDa heat shock protein, HSP90, on glucocorticoid receptor binding to DNA-Cellulose.
- Neutrophil elastase produces 52-kD and 30-kD glucocorticoid receptor fragments in the cytosol of human Leukemia cells.
- Evidence for intraCellular association of the glucocorticoid receptor with the 90-kDa heat shock protein.
- Glucocorticoid-induced DNA fragmentation in acute lymphoblastic Leukemia cells.
- Glucocorticosteroids induce DNA fragmentation in human lymphoid Leukemia cells.
- Role of nicotinamide adenine dinucleotide and adenosine triphosphate in glucocorticoid-induced cytotoxicity in susceptible lymphoid Cells.
- Kinetic pulse-chase labeling study of the glucocorticoid receptor in mouse Lymphoma cells. Effect of glucocorticoid and antiglucocorticoid hormones on intracellular re...
- Chemotherapy-induced emergencies.
- Metabolic emergencies in clinical oncology.
- Recent insight into the structure and function of the glucocorticoid receptor.
- Mapping the HSP90 binding region of the glucocorticoid receptor.
- Evidence from pulse-chase labeling studies that the antiglucocorticoid hormone RU486 stabilizes the nonactivated form of the glucocorticoid receptor in mouse Lymphoma ...
- Comparison of the 90-kilodalton heat shock protein interaction with in vitro translated glucocorticoid and estrogen receptors.
- Preferential synthesis of the 78-Kd glucose-regulated protein in glucocorticoid-treated S49 mouse Lymphoma cells.
- Glucocorticoids inhibit trypsin-induced DNA release from phytohemagglutinin-stimulated blood lymphocytes.
- Selective release of excreted DNA sequences from phytohemagglutinin-stimulated human peripheral blood lymphocytes. Effects of trypsin and divalent cations.
- Ins(1,4,5)P3-mediated calcium signals and apoptosis: is there a role for Bcl-2?
- Thioredoxin-interacting protein (txnip) is a glucocorticoid-regulated primary response gene involved in mediating glucocorticoid-induced apoptosis.
- Expression of a defective mouse mammary tumor virus envelope glycoprotein precursor which binds stably to GRP78 within the lumen of the endoplasmic reticulum is associ...
- Imidazole antifungals Miconazole and Econazole induce apoptosis in mouse lymphoma and human T cell Leukemia cells: regulation by Bcl-2 and potential role of calcium.
- Selective regulation of IP3-receptor-mediated Ca2+ signaling and apoptosis by the BH4 domain of Bcl-2 versus Bcl-Xl.
- Inhibition of Lck enhances glucocorticoid sensitivity and apoptosis in lymphoid cell lines and in Chronic lymphocytic leukemia.
Schools
Ohio State University College Of Medicine and Public Health
Yale New Haven Med Center
Barnes Jewish Hospital
Washington University
Procedures Preformed
- Cardiac MRI (Magnetic Resonance Imaging) of Heart or Chest
- Thoracentesis
Conditions Treated
- Anemia
- Breast Cancer
- Chronic Myeloid Leukemia (CML)
- Coagulation Disorders (incl. Hemophilia)
- View All
Doctors Specialties
- Hematology
- Oncology
Accepted Insurances
Awards
- Elected Member
Education
-
Washington University - Barnes-Jewish Hospital -
Yale-New Haven Hospital -
The Ohio State University College of Medicine
Hospital
-
University Hospitals Case Medical Center
Drug Facts
| NPI NUMBER | 1669491411 | |
| NPPES Provider LastName | DISTELHORST | |
| NPPES Provider FirstName | CLARK | |
| NPPES Provider ZIPCode | 441061716 | |
| NPPES Provider State | OH | |
| Specialty Description | Hematology/Oncology | |
| Total Claim Count | 57.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1669491411 |
| Last Name Of The Provider | DISTELHORST |
| First Name Of The Provider | CLARK |
| View All |
Similar Doctors
|
Dr. Ramon V. Tiu, MD
 This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Manmeet S. Ahluwalia, MD
This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Pierre L. Triozzi, MD
This Doctor is OpenDoctor Recommended.
 This doctor has more publications
|
|
|
Dr. Poornanand Palaparty, MD
This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Asha Kallianpur, MD
This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Robin L. Miller, MD |
|
|
Dr. Michelle E. Treasure, MD |
|
|
Dr. Tycel J. Phillips, MD
This Doctor is OpenDoctor Recommended.
|