Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda.
- F. Chimienti, R. Hogg, D. Hohl
- BiologyHuman Molecular Genetics
- 15 November 2003
It is found that SLURP-1 potentiates the human alpha 7 nicotinic acetylcholine receptors that are present in keratinocytes and is likely to be essential for both epidermal homeostasis and inhibition of TNF-alpha release by macrophages during wound healing.
Dipeptidyl-peptidase IV secreted by Aspergillus fumigatus, a fungus pathogenic to humans
- A. Beauvais, M. Monod, J. Latgé
- Biology, ChemistryInfection and Immunity
- 1 August 1997
A dipeptidyl- peptidase IV was purified from the culture medium of the human-pathogenic fungus Aspergillus fumigatus and is a secreted enzyme with a cleavable signal peptide.
Cardiac and Vascular Hypertrophy in Fabry Disease: Evidence for a New Mechanism Independent of Blood Pressure and Glycosphingolipid Deposition
- F. Barbey, N. Brakch, D. Hayoz
- Medicine, BiologyArteriosclerosis, Thrombosis and Vascular Biology
- 1 April 2006
LVH and CCA IMT occur concomitantly in Fabry suggesting common pathogenesis, and the underlying cause may be a circulating growth-promoting factor whose presence has been confirmed in vitro.
Kinetic Study of Neuropeptide Y (NPY) Proteolysis in Blood and Identification of NPY3–35
- K. Abid, B. Rochat, E. Grouzmann
- BiologyJournal of Biological Chemistry
- 20 July 2009
Kinetic studies indicated that NPY1–36 is rapidly cleaved in serum into 3 main fragments with the following order of efficacy: NPY3–36 ≫ NPY 3–35 > NPY2–36 > NPy3–35.
Autophagosome maturation is impaired in Fabry disease
- M. Chevrier, N. Brakch, S. Bekri
- Biology, MedicineAutophagy
- 1 July 2010
Findings suggest that Fabry disease is linked to a deregulation of autophagy, with increased basal levels compared to cells from non-Fabry subjects and a larger increase in response to starvation than seen in non- Fabry cells.
Increased carotid intima-media thickness in the absence of atherosclerotic plaques in an adult population with Fabry disease.
Evidence of a major increase in common carotid artery IMT is presented, both in hemizygous and heterozygous patients with Fabry disease, in the absence of focal atherosclerotic plaques, which suggests that the conduit arteries may be protected from atherosclerosis in Faby disease.
Evidence for a role of sphingosine-1 phosphate in cardiovascular remodelling in Fabry disease.
- N. Brakch, O. Dormond, F. Barbey
- Biology, MedicineEuropean Heart Journal
Sphingosine-1 phosphate participates in cardiovascular remodelling in Fabry disease and its findings have implications for the treatment of cardiovascular involvement inFabry disease.
SLURP1 is a late marker of epidermal differentiation and is absent in Mal de Meleda.
- B. Favre, L. Plantard, D. Hohl
- BiologyJournal of Investigative Dermatology
- 1 February 2007
SLURP1 was found to be a marker of late differentiation, predominantly expressed in the granular layer of skin, notably the acrosyringium, suggesting that a simple immunologic test could be used as a rapid screening procedure.
Role of prohormone convertases in pro-neuropeptide Y processing: coexpression and in vitro kinetic investigations.
- N. Brakch, B. Rist, E. Grouzmann
- 23 December 1997
It is proposed that the constitutive secreted NPY does not result from theCleavage carried out by ubiquitously expressed enzymes furin and PACE4; that PC1/3 and PC2 are not equipotent in the cleavage of ProNPY; and substrate peptide length might discriminate PC1-3 andPC2 processing activity.
Loss of dipeptidylpeptidase IV activity in chronic rhinosinusitis contributes to the neurogenic inflammation induced by substance P in the nasal mucosa
- E. Grouzmann, M. Monod, J. Lacroix
- Medicine, BiologyThe FASEB Journal
- 1 July 2002
A new pathophysiological pathway for rhinitis is suggested based on clinical observations in humans, indicating the involvement of an enzyme to modulate non‐adrenergic and non‐cholinergicnon‐ cholinergic substrate that occurred during nasal dysfunctions.