Lysophosphatidic acid mediates the rapid activation of platelets and endothelial cells by mildly oxidized low density lipoprotein and accumulates in human atherosclerotic lesions.
- W. Siess, K. Zangl, M. Aepfelbacher
- BiologyProceedings of the National Academy of Sciences…
- 8 June 1999
This study identifies LPA as an atherothrombogenic molecule and suggests a possible strategy to prevent and treat atherosclerosis and cardiocerebrovascular diseases.
Identification of Bcl-6-dependent follicular helper NKT cells that provide cognate help for B cell responses
In vivo, NKT cells engaged in stable and prolonged cognate interactions with B cells and induced the formation of early germinal centers that demonstrated the existence of a Bcl-6-dependent subset of N KT cells specialized in providing help to B cells.
Effect of the Structure of Natural Sterols and Sphingolipids on the Formation of Ordered Sphingolipid/Sterol Domains (Rafts)
- Xiaolian Xu, R. Bittman, G. Duportail, D. Heissler, C. Vilchèze, E. London
- Biology, ChemistryJournal of Biological Chemistry
- 7 September 2001
It was found that a small amount of ceramide significantly stabilized domain/raft formation and the molecular basis for, and the implications of, the effects of different sterols and sphingolipids on the behavior and biological function of rafts are discussed.
Erythrocytes serve as a reservoir for cellular and extracellular sphingosine 1‐phosphate
- C. Bode, Sven‐Christian Sensken, M. Gräler
- Biology, MedicineJournal of Cellular Biochemistry
- 15 April 2010
RBC‐associated S1P has two functions: (1) It contributes to the cellular pool of SGPL1‐sensitive S 1P in tissues after transcellular transportation and (2) it helps maintain extracellular S1p levels via SA and HDL independently fromSGPL1 activity.
Lysophosphatidic Acid Induces Neointima Formation Through PPARγ Activation
Exposure to brief exposure to either alkyl ether analogs of the growth factor–like phospholipid lysophosphatidic acid (LPA), products generated during the oxidative modification of low density lipoprotein, or to unsaturated acyl forms of LPA induce progressive formation of neointima in vivo in a rat carotid artery model suggests selected LPA analogs are important novel endogenous PPARγ ligands capable of mediating vascular remodeling.
Crystal Structure of the Mycobacterium tuberculosis Enoyl-ACP Reductase, InhA, in Complex with NAD+ and a C16 Fatty Acyl Substrate*
- D. A. Rozwarski, C. Vilchèze, M. Sugantino, R. Bittman, J. Sacchettini
- Chemistry, BiologyJournal of Biological Chemistry
- 28 May 1999
The crystal structure of InhA in complex with NAD+ and a C16 fatty acyl substrate,trans-2-hexadecenoyl-(N-acetylcysteamine)-thioester, reveals that the substrate binds in a general “U-shaped” conformation, consistent with the ability of InHA to recognize longer chain fatty acy substrates.
Structural Elucidation of the Specificity of the Antibacterial Agent Triclosan for Malarial Enoyl Acyl Carrier Protein Reductase*
The cloning and expression of the P. falciparum enoyl acyl carrier protein reductase gene is reported, which encodes a 50-kDa protein (PfENR) predicted to target to the unique parasite apicoplast, and the structural basis of triclosan binding to PfENR is defined, which will facilitate structure-based optimization of Pf ENR inhibitors.
FTY720 and (S)-FTY720 vinylphosphonate inhibit sphingosine kinase 1 and promote its proteasomal degradation in human pulmonary artery smooth muscle, breast cancer and androgen-independent prostate…
NADH Dehydrogenase Defects Confer Isoniazid Resistance and Conditional Lethality in Mycobacterium smegmatis
- L. Miesel, T. Weisbrod, J. Marcinkeviciene, R. Bittman, W. Jacobs
- BiologyJournal of Bacteriology
- 1 May 1998
The genetic data presented here indicate that defects in NADH oxidation cause all of the mutant traits and that an increase in the NADH/NAD+ ratio confers INH resistance.
Enzymatic characterization of the target for isoniazid in Mycobacterium tuberculosis.
Kinetic and microcalorimetric analysis demonstrates that the binding of NADH to the S94A mutant InhA, known to confer resistance to both isoniazid and ethionamide, is altered, with the formation of a binary InHA-NADH complex required for drug binding.