Head of Laboratory, Assistant Professor
Pathology
Dr. Agata M. Smogorzewska, MD
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Agata Smogorzewska works in the field of Pathology. She went to medical school at Weill Cornell Medical College of Cornell University. Weill Cornell Medical College of Cornell University is ranked 18 in research and 49 in primary care medicine Agata Smogorzewska is also a published MD. She has 39 paper published. The most recent paper is: TRF2 protects human telomeres from end-to-end fusions.
Publications
- Paternal or Maternal Uniparental Disomy of Chromosome 16 Resulting in Homozygosity of a Mutant Allele Causes Fanconi Anemia.
- Natural history and management of Fanconi anemia patients with head and neck cancer: A 10 year follow-up.
- SnapShot: fanconi anemia and associated proteins.
- Noncovalent Interactions with SUMO and Ubiquitin Orchestrate Distinct Functions of the SLX4 Complex in Genome Maintenance.
- Comprehensive Analysis of Pathogenic Deletion Variants in Fanconi Anemia Genes.
- Human GEN1 and the SLX4-Associated Nucleases MUS81 and SLX1 Are Essential for the Resolution of Replication-Induced Holliday Junctions.
- Massively parallel sequencing, ArrayCGH and RNA-Seq technologies provide a comprehensive molecular diagnosis of Fanconi anemia.
- Fanconi anaemia and the repair of Watson and Crick DNA crosslinks.
- Regulation of multiple DNA repair pathways by the Fanconi anemia protein SLX4.
- Assessment of SLX4 Mutations in Hereditary Breast Cancers.
- Partial MCM4 deficiency in patients with growth retardation, adrenal insufficiency, and natural killer cell deficiency.
- A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage response.
- Postoperative clinical radiosensitivity in patients with fanconi anemia and head and neck squamous cell carcinoma.
- Structure of the FANCI-FANCD2 complex: insights into the Fanconi anemia DNA repair pathway.
- Ubiquitylation and the Fanconi anemia pathway.
- Mutations of the SLX4 gene in Fanconi anemia.
- Polybromo-associated BRG1-associated factor components BRD7 and BAF180 are critical regulators of p53 required for induction of replicative senescence.
- A genetic screen identifies FAN1, a Fanconi anemia-associated nuclease necessary for DNA interstrand crosslink repair.
- The Fanconi anemia pathway promotes replication-dependent DNA interstrand cross-link repair.
- Mammalian BTBD12/SLX4 assembles a Holliday junction resolvase and is required for DNA repair.
- FANCI phosphorylation functions as a molecular switch to turn on the Fanconi anemia pathway.
- Cancer proliferation gene discovery through functional genomics.
- Abraxas and RAP80 form a BRCA1 protein complex required for the DNA damage response.
- ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage.
- Identification of the FANCI protein, a monoubiquitinated FANCD2 paralog required for DNA repair.
- Postmortem urine immunoassay showing false-positive phencyclidine reactivity in a case of fatal tramadol overdose.
- Effect of fondaparinux on coagulation assays: results of College of American Pathologists proficiency testing.
- Transfusion medicine illustrated. Volume-reduced apheresis platelets.
- Homologous recombination generates T-loop-sized deletions at human telomeres.
- Paraprotein interference in automated chemistry analyzers.
- Regulation of telomerase by telomeric proteins.
- DNA damage foci at dysfunctional telomeres.
- DNA ligase IV-dependent NHEJ of deprotected mammalian telomeres in G1 and G2.
- Different telomere damage signaling pathways in human and mouse cells.
- Senescence induced by altered telomere state, not telomere loss.
- Control of human telomere length by TRF1 and TRF2.
- TRF2 protects human telomeres from end-to-end fusions.
- Human telomeres contain two distinct Myb-related proteins, TRF1 and TRF2.
Schools
Weill Cornell Medical College
Doctors Specialties
- Pathology
Accepted Insurances
Education
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Massachusetts General Hospital -
Weill Cornell Medical College of Cornell University
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