Daniel S. O’Connor

ORCID: 0009-0003-0011-0779
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Cell death mechanisms and regulation
  • Prostate Cancer Treatment and Research
  • Congenital Heart Disease Studies
  • Radiopharmaceutical Chemistry and Applications
  • Cancer-related Molecular Pathways
  • Microtubule and mitosis dynamics
  • Pulmonary Hypertension Research and Treatments
  • Estrogen and related hormone effects
  • Acute Lymphoblastic Leukemia research
  • Cell Adhesion Molecules Research
  • COVID-19 Clinical Research Studies
  • COVID-19 and healthcare impacts
  • Angiogenesis and VEGF in Cancer
  • Cardiac Valve Diseases and Treatments
  • Adipokines, Inflammation, and Metabolic Diseases
  • HER2/EGFR in Cancer Research
  • Caveolin-1 and cellular processes
  • Ion Transport and Channel Regulation
  • Long-Term Effects of COVID-19
  • Sepsis Diagnosis and Treatment
  • Chronic Lymphocytic Leukemia Research
  • Pancreatitis Pathology and Treatment
  • Cardiac tumors and thrombi
  • Kawasaki Disease and Coronary Complications
  • Legal Systems and Judicial Processes

Ambrx (United States)
2024

Columbia University Irving Medical Center
2011-2023

Beaumont Health
2020

Beaumont Hospital, Royal Oak
2020

NewYork–Presbyterian Hospital
2011-2017

Columbia University
2013-2017

University of California, San Francisco
2013

New York Hospital Queens
2011

Yale University
2000-2002

A productive angiogenic response must couple to the survival machinery of endothelial cells preserve integrity newly formed vessels. Angiopoietin-1 (Ang-1) is an endothelium-specific ligand essential for embryonic vascular stabilization, branching morphogenesis, and post-natal angiogenesis, but its contribution cell has not been completely elucidated. Here we show that Ang-1 acting via Tie 2 receptor induces phosphorylation serine-threonine kinase, Akt (or protein kinase B). This associated...

10.1074/jbc.275.13.9102 article EN cc-by Journal of Biological Chemistry 2000-03-01

The interface between apoptosis (programmed cell death) and the cycle is essential to preserve homeostasis genomic integrity. Here, we show that survivin, an inhibitor of over-expressed in cancer, physically associates with cyclin-dependent kinase p34 cdc2 on mitotic apparatus, phosphorylated Thr 34 by -cyclin B1, vitro vivo . Loss phosphorylation resulted dissociation a survivin-caspase-9 complex caspase-9-dependent cells traversing mitosis. These data identify survivin as substrate B1...

10.1073/pnas.240390697 article EN Proceedings of the National Academy of Sciences 2000-11-07

Higher comorbidity and older age have been reported as correlates of poor outcomes in COVID-19 patients worldwide; however, US data are scarce. We evaluated mortality predictors a large cohort hospitalized the United States. Retrospective, multicenter inpatients diagnosed with by RT-PCR from 1 March to 17 April 2020 was performed, outcome 2020. Measures included demographics, comorbidities, clinical presentation, laboratory values imaging on admission. Primary mortality. Secondary length...

10.1111/joim.13119 article EN Journal of Internal Medicine 2020-06-04

10.1016/s1535-6108(02)00084-3 article EN publisher-specific-oa Cancer Cell 2002-07-01

The activity of endothelial nitric-oxide synthase (eNOS) is regulated by its subcellular localization, phosphorylation and through interaction with different proteins. association eNOS caveolin-1 (Cav) believed to maintain in an inactive state; however, increased heat shock protein 90 (hsp90) observed following activation. In this study, we investigate the relationship between caveolin hsp90 as opposing regulatory proteins on function. Immunoprecipitation Cav-1 from bovine lung microvascular...

10.1074/jbc.m001644200 article EN cc-by Journal of Biological Chemistry 2000-07-01

Survivin is a member of the inhibitor apoptosis gene family that has been implicated in both inhibition and regulation mitosis. However, subcellular distribution survivin controversial variously described as microtubule-associated protein or chromosomal passenger protein. Here, we show antibodies directed to sequence Ala3-Ile19 exclusively recognized nuclear pool segregated with nucleoplasmic proteins, but not outer matrix proteins. By immunofluorescence,nuclear localized kinetochores...

10.1242/jcs.115.3.575 article EN Journal of Cell Science 2002-02-01

Metastatic castration-resistant prostate cancer (mCRPC) is an advanced disease in which patients ultimately fail standard-of-care androgen deprivation therapies and exhibit poor survival rates. The prostate-specific membrane antigen (PSMA) has been validated as mCRPC tumor with overexpression tumors low expression healthy tissues. Using our proprietary technology for incorporating synthetic amino acids into proteins at selected sites, we have developed ARX517, antibody-drug conjugate...

10.1158/1535-7163.mct-23-0927 article EN cc-by-nc-nd Molecular Cancer Therapeutics 2024-08-22

10.1016/j.jcct.2011.04.001 article EN Journal of cardiovascular computed tomography 2011-04-24

<div>Abstract<p>Metastatic castration-resistant prostate cancer (mCRPC) is an advanced disease in which patients ultimately fail standard-of-care androgen deprivation therapies and exhibit poor survival rates. The prostate-specific membrane antigen (PSMA) has been validated as mCRPC tumor with overexpression tumors low expression healthy tissues. Using our proprietary technology for incorporating synthetic amino acids into proteins at selected sites, we have developed ARX517,...

10.1158/1535-7163.c.7567771 preprint EN 2024-12-03

<p>ARX517 is stable over 21-day incubation in human serum. ARX517 was incubated for the indicated times at 37C, 5% CO2 pooled Time point samples were quantified Total Ab (TA) and Intact ADC assay to assess stability.</p>

10.1158/1535-7163.27951232 preprint EN cc-by 2024-12-03

Abstract Tyrosine kinases inhibitors induce genotype-specific regression in advanced human cancers. However, these responses are almost invariably transient and patients ultimately relapse due to outgrowth of drug-resistant clones. Thus, increased knowledge the mechanisms underlying de novo acquired resistance is essential for enhancing clinical efficacy. T cell acute lymphoblastic leukemia (T-ALL) an aggressive cancer which current therapies toxic frequently ineffective. Mutations genes...

10.1158/1538-7445.am2013-4448 article EN Cancer Research 2013-04-01
Coming Soon ...