The effect of ascorbic acid on β-glycerophosphate

Thannhauser, S. J.; Reichel, Max; Grattan, Jerome F.

doi:10.1042/bj0321163

Cited by 13 publications

(3 citation statements)

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“…Acid sphingomyelinase (ASM; EC 3.1.4.12) is one member of a family of enzymes that catalyzes the breakdown of sphingomyelin by cleavage of the phosphorylcholine linkage, thereby producing ceramide. The existence of such a ''sphingomyelin cleaving enzyme" was first demonstrated in 1938 by the pioneering work of Thannhauser, Reichel and colleagues [9]. During the ensuing 25 years, several similar enzymatic activities were identified that differed mostly in their tissue distribution and pH optimum.…”

Section: Acid Sphingomyelinase: Historical Perspectivementioning

confidence: 99%

Acid sphingomyelinase, cell membranes and human disease: Lessons from Niemann–Pick disease

2009

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a b s t r a c tAcid sphingomyelinase (ASM) plays an important role in normal membrane turnover through the hydrolysis of sphingomyelin, and is one of the key enzymes responsible for the production of ceramide. ASM activity is deficient in the genetic disorder Types A and B Niemann-Pick disease (NPD). ASM knockout (ASMKO) mice were originally constructed to study this disorder, and numerous defects in ceramide-related signaling have been shown. Studies in these mice have further suggested that ASM may be involved in the pathogenesis of several common diseases through the reorganization of membrane microdomains. This review will focus on the role of ASM in membrane biology, with a specific emphasis on what a rare genetic disorder (NPD) has taught us about more common events.

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Section: Acid Sphingomyelinase: Historical Perspectivementioning

confidence: 99%

Acid sphingomyelinase, cell membranes and human disease: Lessons from Niemann–Pick disease

2009

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“…Thannhauser and his associates have interpreted their clinical and experimental studies (18,19) to signify that the increased serum phosphatase activity observed in sundry diseases, including obstructive jaundice, is due not to increased concentration of the enzyme in the blood but rather to the effect of an activator on the enzyme. This hypothesis is based upon their observation that ascorbic acid activates serum phosphatase (20), a phenomenon subsequent studies (21,22) proved to be an artefact. The activity of "alkaline" phosphatase is slightly inhibited by bile salts (23).…”

Section: Cirrhosis Of the Livermentioning

confidence: 99%

“…MFay 20,1937 June 14, 1937 November 13,1936 April 20, 1938 Way 16, 1938 August 11,1938 December 2, 1936 December 22, 1936 November 22, 1937 December 1, 1937 May 31, 1938 January 13, 1937 January 12, 1937 January 20, 1937 March 24, 1939 March 31, 1939 January 27, 1939 February 15, 1939 March 14,1939 October 28, 1938 November 28,1938 December 15, 1938 January 25, 1939 …”

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confidence: 99%