Genomes and Genes
Affiliation: New York University School of Medicine
- Drug-induced myopathiesAdam Mor
Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA
Bull NYU Hosp Jt Dis 67:358-69. 2009..Earlier diagnosis and drug discontinuation raises the likelihood of resolution and recovery...
- Inhibition of contact sensitivity by farnesylthiosalicylic acid-amide, a potential Rap1 inhibitorAdam Mor
Department of Medicine, New York University School of Medicine, New York, New York, USA
J Invest Dermatol 131:2040-8. 2011..Moreover, FTS-A inhibited Rap1 and contact sensitivity far better than FTS. We suggest that FTS-A may serve as a possible therapeutic tool in contact sensitivity in particular and T-cell-mediated inflammation in general...
- Immunomodulatory properties of farnesoids: the new steroids?A Mor
Department of Medicine, New York University School of Medicine, 450 E 29th Street, New York, NY 10016, USA
Curr Med Chem 20:1218-24. 2013..In this review we summarize our (and others) published data, and conclude that FTS has great potential as a safe anti-inflammatory drug...
- Celecoxib enhances the anti-inflammatory effects of farnesylthiosalicylic acid on T cells independent of prostaglandin E(2) productionAdam Mor
Department of Medicine, Division of Rheumatology, New York University School of Medicine, 450 E 29th Street, New York, NY 10016, USA
Inflammation 35:1706-14. 2012..The inhibitory effects, moreover, were independent of prostaglandin E(2) secretion. These data point to the promising potential of combined treatment with celecoxib and FTS for inflammatory disorders involving lymphocytes...
- Inhibitory effect of farnesylthiosalicylic acid on mediators release by mast cells: preferential inhibition of prostaglandin D(2) and tumor necrosis factor-α releaseAdam Mor
Department of Neurobiology, The George Weise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, 61390, Israel
Inflammation 34:314-8. 2011..This data suggests that FTS may have an inhibitory effect on MC mediated allergic inflammation, and thus may be considered as a possible therapeutic modality...
- Characterization of ERK activation in human mast cells stimulated by contact with T cellsAdam Mor
The Laboratory of Allergy and Clinical Immunology, Meir Medical Center, Kfar Saba, Israel
Inflammation 33:119-25. 2010..Thus, retaining ERK in the nucleus might be a mechanism utilized by human mast cells to generate different cytokines from a single signaling cascade...
- T cell-induced mast cell activation: a role for microparticles released from activated T cellsIrit Shefler
Laboratory of Allergy and Clinical Immunology, Department of Medicine, Meir Medical Center, Kfar Saba, Israel
J Immunol 185:4206-12. 2010..By extension, microparticles might affect the activity of mast cells, which are usually not in direct contact with T cells at the inflammatory site...
- Phospholipase D1 regulates lymphocyte adhesion via upregulation of Rap1 at the plasma membraneAdam Mor
The Cancer Institute, NYU School of Medicine, New York, New York 10016, USA
Mol Cell Biol 29:3297-306. 2009..Our data support a model whereby PLD1 regulates Rap1 activity by controlling exocytosis of a stored, vesicular pool of Rap1 that can be activated by C3G upon delivery to the plasma membrane...
- Rap1-interacting adapter molecule (RIAM) associates with the plasma membrane via a proximity detectorJoseph P Wynne
Cancer Institute, NYU School of Medicine, New York, NY 10016, USA
J Cell Biol 199:317-30. 2012..Thus, the RA-PH domains of RIAM function as a proximity detector for activated Rap1 and PI(4,5)P(2)...
- Cytotoxic-T-lymphocyte antigen 4 receptor signaling for lymphocyte adhesion is mediated by C3G and Rap1Yoel Kloog
Department of Neurobiology, George S Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel
Mol Cell Biol 34:978-88. 2014..These findings point to C3G and Hck as promising potential therapeutic targets for the treatment of T-cell-dependent autoimmune disorders. ..
- Drugs causing muscle diseaseAdam Mor
Division of Rheumatology, Department of Medicine, New York University School of Medicine, 301 East 17th Street Room 1410, New York, NY 10003, USA
Rheum Dis Clin North Am 37:219-31, vi. 2011..In this article, some of the commonly used drugs that may induce myopathies, as well as the clinical phenotypes, diagnosis, and management of these syndromes are reviewed...
- Ras chaperones: new targets for cancer and immunotherapyYoel Kloog
Department of Neurobiology, Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Israel Electronic address
Enzymes 33:267-89. 2013..We conclude that FTS has a great potential both as a safe anticancer drug and as a promising immune modulator agent. ..
- Small GTPases and LFA-1 reciprocally modulate adhesion and signalingAdam Mor
Department of Medicine, NYU School of Medicine, New York, NY 10016, USA
Immunol Rev 218:114-25. 2007..We have recently shown that Ras is also downstream of LFA-1 engagement: LFA-1 signaling through phospholipase D (PLD) to RasGRP1 was required for Ras activation on the plasma membrane following stimulation of TCR...
- Familial Mediterranean fever successfully treated with etanerceptAdam Mor
Department of Medicine, Division of Rheumatology, New York University School of Medicine Hospital for Joint Diseases, New York, NY 10003, USA
J Clin Rheumatol 13:38-40. 2007..This case adds to a growing body of evidence suggesting that tumor necrosis factor (TNF) blockade may result in resolution and prevention of further FMF attacks...
- The lymphocyte function-associated antigen-1 receptor costimulates plasma membrane Ras via phospholipase D2Adam Mor
Department of Medicine, NYU School of Medicine, New York, NY 10016, USA
Nat Cell Biol 9:713-9. 2007..PLD2 and phosphatidic acid phosphatase (PAP) were required for Ras activation on the plasma membrane. Thus, LFA-1 acts through PLD2 to reshape the pattern of Ras activation downstream of the TCR...
- Topology of mammalian isoprenylcysteine carboxyl methyltransferase determined in live cells with a fluorescent probeLatasha P Wright
NYU Cancer Institute and Departments of Medicine, Cell Biology, and Pharmacology, NYU School of Medicine, New York, New York 10016, USA
Mol Cell Biol 29:1826-33. 2009..Icmt is a target for anticancer drug discovery, and these data may facilitate efforts to develop small-molecule inhibitors...
- Drug-induced arthritic and connective tissue disordersAdam Mor
Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, NY 10003, USA
Semin Arthritis Rheum 38:249-64. 2008..We assess the strength of the reported associations, discuss diagnostic features and treatment implications, and consider possible mechanisms for drug-induced genesis of rheumatic conditions...
- The role of Ras signaling in lupus T lymphocytes: biology and pathogenesisAdam Mor
Department of Medicine, Division of Rheumatology, New York University School of Medicine, the NYU Hospital for Joint Diseases, NY 10003, USA
Clin Immunol 125:215-23. 2007..In this manuscript, we review the basic biology of Ras in T lymphocytes, and the ways in which T lymphocyte Ras abnormalities may contribute to the development of a lupus phenotype...
- Neurologic manifestations as presenting symptoms of endocarditisAdaya Weissler
Department of Medicine, Meir Medical Center, Kfar Saba, affiliated with Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel
Isr Med Assoc J 12:472-6. 2010..A prompt diagnosis should be reached and antibiotic treatment initiated as soon as possible...
- Cellular therapy in 2010: focus on autoimmune and cardiac diseasesLeor Perl
Department of Medicine B, Meir Medical Center, Kfar Saba, Israel
Isr Med Assoc J 12:110-5. 2010....
- Structure-function analysis of nucleolin and ErbB receptors interactionsKeren Farin
Department of Neurobiology, Tel Aviv University, Ramat Aviv, Israel
PLoS ONE 4:e6128. 2009..Recently we have found that cell-surface ErbB receptors interact with nucleolin via their cytoplasmic tail. Overexpression of ErbB1 and nucleolin leads to receptor phosphorylation, dimerization and anchorage independent growth...
- Autoimmunity and mast cell-related diseasesEyal Reinstein
Instructor of Medicine, Department of Medicine B, Meir General Hospital, Kfar Saba, 44281, Israel and, The Sackler School of Medicine, Tel Aviv University, Israel
Expert Rev Clin Immunol 4:267-74. 2008..The involvement of the main effectors of the immune system - mast cells, T lymphocytes, antibodies and cytokines - in both conditions is also discussed...
- Syphilis mimicking Reiter's syndrome in an HIV-positive patientMitsumasa Kishimoto
Division of Rheumatology, NYU School of Medicine Hospital for Joint Diseases, New York, New York 10016, USA
Am J Med Sci 332:90-2. 2006..Because the initial presentation was difficult to distinguish from the symptoms of Reiter's syndrome, a high degree of clinical suspicion was required to accurately diagnose syphilis, a curable and potentially fatal disease...
- Relapsing oligoarticular septic arthritis during etanercept treatment of rheumatoid arthritisAdam Mor
Division of Rheumatology, New York University School of Medicine Hospital for Joint Diseases, 301 East 17th Street, Rm 1410, New York, NY 10003, USA
J Clin Rheumatol 12:87-9. 2006..Our case underscores the advisability of discontinuing TNF-alpha blockade in patients with septic arthritis during prolonged antimicrobial therapy...
- Compartmentalized Ras/MAPK signalingAdam Mor
Department of Medicine, New York University Medical Center, New York, NY 10016 6402, USA
Annu Rev Immunol 24:771-800. 2006..Thus, the Ras/MAPK pathway represents a clear example of compartmentalized signaling...
- PKC regulates a farnesyl-electrostatic switch on K-Ras that promotes its association with Bcl-XL on mitochondria and induces apoptosisTrever G Bivona
Department of Cell Biology, New York University School of Medicine, 550 First Avenue, New York, New York 10016, USA
Mol Cell 21:481-93. 2006..These data demonstrate that the location and function of K-Ras are regulated directly by PKC and suggest an approach to therapy of K-Ras-dependent tumors with agents that stimulate phosphorylation of S181...