Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study demonstrates a procedure for extraction and determination of stratum corneum amines in the living animal. A nonleaky well, containing 10 mM Tris-HCl buffer, pH 7.0, was constructed on the shaved backs of anesthetized animals. It was found that Ser, Ala, Gly and Pro are mainly released from the stratum corneum of 4-month-old guinea pigs, and in 2-month-old rats, Gly, Ser and Arg show the highest degree of release. Much lower amino acid concentrations were observed in 20-month-old rats. This was also reflected by the high levels of fluorescamine-reactive substances released from young rat skin as compared to the old animals. The release of the neuropeptide substance P into the aqueous medium was increased 3.2 times upon heat stimulus as compared to control skin. Amines and other compounds released from the skin may serve as markers for skin aging or for certain skin disorders, leading to a new approach for their treatments.
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PMID:Release of amino acids, fluorescamine-reactive substances and substance P from the epidermis of the living animal. 1032 89

Alzheimer's disease (AD) is primarily nonfamilial or sporadic (SAD) in origin, although several genetic linkages are reported. Tissues from AD patients contain fibrillar plaques made of 39 to 43 amino acid-long amyloid beta peptide (AbetaP), although the mechanisms of AbetaP toxicity are poorly understood. AbetaP(1-40) is the most prevalent AbetaP present in the neuronal and non-neuronal tissues from SAD patients. AbetaP(1-40) toxicity has been examined mainly after prolonged incubation and correlates with the age and fibrillar morphology of AbetaP(1-40). Globular and nonfibrillar AbetaPs are released continually during normal cellular metabolism; they elevate cellular Ca(2+) and form cation-permeable channels. However, their role in cellular toxicity is poorly understood. We have used an integrated atomic force and light fluorescence microscopy (AFM-LFM), laser confocal microscopy, and calcium imaging to examine real-time and acute effect of fresh and globular AbetaP(1-40) on cultured, aged human, AD-free fibroblasts. AFM images show that freshly prepared AbetaP(1-40) in phosphate-buffered saline (PBS) are globular and do not form fiber for an extended time period. AbetaP(1-40) induced rapid structural modifications, including cytoskeletal reorganization, retraction of cellular processes, and loss of cell-cell contacts, within minutes of incubation. This led to eventual cellular degeneration. AbetaP(1-40)-induced degeneration was prevented by anti-AbetaP antibody, zinc, and Tris, but not by tachykinin neuropeptides. In Ca(2+)-free extracellular medium, AbetaP(1-40) did not induce cellular degeneration. In the presence of extracellular Ca(2+), AbetaP(1-40) induced a sustained increase in the cellular Ca(2+). Thus, short-term and acute AbetaP(1-40) toxicity is mediated by Ca(2+) uptake, most likely via calcium-permeable AbetaP pores. Such rapid degeneration does not require fibrillar plaques, suggesting that the plaques may not have any causative role.
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PMID:Fresh and nonfibrillar amyloid beta protein(1-40) induces rapid cellular degeneration in aged human fibroblasts: evidence for AbetaP-channel-mediated cellular toxicity. 1083 46


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