Professor, Medicine, University of Washington School of Medicine
Oncology
Dr. Bruce E. Clurman, MD
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Bruce Clurman practices Oncology. Bruce E. Clurman is a published MD. He has 61 papers published. The most current publication "New insights into the tumor suppression function of P27(kip1)"
Publications
- Mislocalization of p27 to the cytoplasm of Breast cancer cells confers resistance to anti-HER2 targeted therapy.
- Oncoprotein ubiquitylation: Dimers, degrons, and degradation.
- Essential role for Cdk2 inhibitory phosphorylation during replication stress revealed by a human Cdk2 knockin mutation.
- Cand1 Promotes Assembly of New SCF Complexes through Dynamic Exchange of F Box Proteins.
- Phosphorylation of eukaryotic elongation factor 2 (eEF2) by cyclin A-cyclin-dependent kinase 2 regulates its inhibition by eEF2 kinase.
- Fbw7 and p53 cooperatively suppress advanced and chromosomally unstable intestinal Cancer.
- Hypoxia inducible factor-1 is activated by dysregulated cyclin E during mammary epithelial morphogenesis.
- Nucleolar targeting of the fbw7 ubiquitin ligase by a pseudosubstrate and glycogen synthase kinase 3.
- Effect of Xpcl1 activation and p27(Kip1) loss on gene expression in murine Lymphoma.
- Mass spectrometry-based identification of protein kinase substrates utilizing engineered kinases and thiophosphate labeling.
- Isoform- and Cell cycle-dependent substrate degradation by the Fbw7 ubiquitin ligase.
- Cyclin E phosphorylation regulates Cell proliferation in hematopoietic and epithelial lineages in vivo.
- A mechanism misregulating p27 in Tumors discovered in a functional genomic screen.
- Hematopoietic cell transplantation in patients with myelodysplastic syndrome or Acute myeloid leukemia arising from myelodysplastic syndrome: similar outcomes in patie...
- FBW7 mutations in leukemic Cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors.
- Discovery of an oncogenic activity in p27Kip1 that causes stem Cell expansion and a multiple tumor phenotype.
- Ubiquitin-independent degradation of Cell-cycle inhibitors by the REGgamma proteasome.
- Kinase-independent function of cyclin E.
- Zcchc8 is a glycogen synthase kinase-3 substrate that interacts with RNA-binding proteins.
- Mechanisms of tumor suppression by the SCF(Fbw7).
- Ras activity regulates cyclin E degradation by the Fbw7 pathway.
- A mouse model for cyclin E-dependent genetic instability and tumorigenesis.
- The SV40 large T antigen contains a decoy phosphodegron that mediates its interactions with Fbw7/hCdc4.
- Terminal osteoblast differentiation, mediated by runx2 and p27KIP1, is disrupted in osteosarcoma.
- N-acetylation and ubiquitin-independent proteasomal degradation of p21(Cip1).
- Recognition of phosphodegron motifs in human cyclin E by the SCF(Fbw7) ubiquitin ligase.
- Notch activation induces endothelial Cell cycle arrest and participates in contact inhibition: role of p21Cip1 repression.
- The Fbw7 tumor suppressor regulates glycogen synthase kinase 3 phosphorylation-dependent c-Myc protein degradation.
- Multisite phosphorylation by Cdk2 and GSK3 controls cyclin E degradation.
- Werner syndrome protein limits MYC-induced Cellular senescence.
- Identification of oncogenes collaborating with p27Kip1 loss by insertional mutagenesis and high-throughput insertion site analysis.
- Npap60/Nup50 is a tri-stable switch that stimulates importin-alpha:beta-mediated nuclear protein import.
- p53 and SCFFbw7 cooperatively restrain cyclin E-associated genome instability.
- Fbw7/hCDC4 dimerization regulates its substrate interactions.
- Analysis of gene expression, copy number and palindrome formation with a Dt40 enriched cDNA microarray.
- FBW7 ubiquitin ligase: a tumour suppressor at the crossroads of Cell division, growth and differentiation.
- Identification of CDK2 substrates in human Cell lysates.
- Transvection mediated by the translocated cyclin D1 locus in mantle cell Lymphoma.
- A nucleolar isoform of the Fbw7 ubiquitin ligase regulates c-Myc and Cell size.
- Cyclin E in normal and neoplastic Cell cycles.
- Cell cycle: how cyclin E got its groove back.
- Cycling without CDK2?
- Regulation of cell proliferation in a stratified culture system of epithelial cells from proState tissue.
- p53 and p21 form an inducible barrier that protects Cells against cyclin E-cdk2 deregulation.
- Curative therapy of advanced essential thrombocythemia or polycythemia vera by hemopoietic stem Cell transplantation.
- Characterization and targeted disruption of murine Nup50, a p27(Kip1)-interacting component of the nuclear pore complex.
- Nup50, a nucleoplasmically oriented nucleoporin with a role in nuclear protein export.
- Proteasomal turnover of p21Cip1 does not require p21Cip1 ubiquitination.
- Cyclin E-CDK2 is a regulator of p27Kip1.
- Turnover of cyclin E by the ubiquitin-proteasome pathway is regulated by cdk2 binding and cyclin phosphorylation.
- Cell cycle and Cancer.
- Multiple proto-oncogene activations in avian leukosis virus-induced Lymphomas: evidence for stage-specific events.
- New insights into the tumor suppression function of P27(kip1)
- Cleavage of p21Cip1/Waf1 and p27Kip1 mediates apoptosis in endothelial Cells through activation of Cdk2: role of a caspase cascade.
- The CDKN2A tumor-suppressor locus--a tale of two proteins.
- Deregulation of Cell cycle control in hematologic malignancies.
- Molecular pathogenesis of myc-initiated B-cell Lymphomas in the bursa of Fabricius.
- Tumour-suppressor genes. Killer in search of a motive?
- Cullin-3 targets cyclin E for ubiquitination and controls S phase in mammalian Cells.
- p73 mutations and expression in adult de novo Acute myelogenous leukemia.
Schools
Weill Cornell Medical College
Brigham and Women39s Hospital
Fred Hutchinson Cancer Res Center
Procedures Preformed
- HPC Transplantation (Stem Cell Transplant)
Conditions Treated
- Acute Leukemia
- Anemia
- Breast Cancer
- Burkitt's Lymphoma
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Doctors Specialties
- Medical Oncology
- Oncology
Accepted Insurances
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1780769588 |
| Last Name Of The Provider | CLURMAN |
| First Name Of The Provider | BRUCE |
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