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Detail of "16758-34-2"

  • CAS Number:
  • 16758-34-2
  • Name:
  • β-D-Galactopyranoside, phenyl1-thio-

  • Molecular Structure:
  • Formula:
  • C12H16O5S
  • Molecular Weight:
  • 272.32
  • Synonyms:
  • Galactopyranoside,phenyl 1-thio-, b-D-(6CI,8CI);Phenyl 1-thio-β-D-galactopyranoside;Phenyl 1-thio-β-D-galactoside;(2R,3R,4S,5R,6S)-2-(Hydroxymethyl)-6-phenylsulfanyloxane-3,4,5-triol;
  • EINECS:
  • 240-818-7
  • Density:
  • 1.48 g/cm3
  • Boiling Point:
  • 510.7 °C at 760 mmHg
  • Flash Point:
  • 262.6 °C

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CAS No.16758-34-2 β-D-Galactopyranoside, phenyl1-thio-

Supplier:Toroma Organics Ltd. [ Germany]

600Integral
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Tel:+49(0)681 / 9592852

Address:66123 Saarbruecken

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Reference

Galactoside-proton symport in a lac YUN mutant of Escherichia coli investigated by analysis of transport progress curves
Galactoside-proton symport in a lac YUN mutant of Escherichia coli investigated by analysis of transport progress curves. Page, Malcolm G. P. (Dep. Microbiol., Biozent., Basel CH-4056, Switz.). Biochem. J., 242(2), 539-50 (English) 1987. CODEN: BIJOAK. ISSN: 0306-3275. DOCUMENT TYPE: Journal CA Section: 10 (Microbial Biochemistry) The kinetics of galactoside-proton symport catalyzed by a wild-type strain and one carrying a mutation, previously reported to cause uncoupling of the symport reaction, were examd. The mutation does not affect the stoichiometry during the initial period of uptake, when the internal concn. of galactoside is low, but it does result in much greater competition from the galactoside as it is accumulated. Simple methods for the anal. of the uptake progress curves were developed and used to est. 155-30-6 and 16758-34-2 which are cas registry numbers of substances are two of reagents here. the initial rate of uptake and affinity for internal galactoside. The max. rate of uptake is decreased by a factor of 2 at most, whereas the affinity for internal galactoside is increased up to 50-fold by the mutation. The pH dependence of the galactoside efflux reaction is changed in a manner which suggests that the defect is in the interaction between proton-binding and galactoside-binding sites rather than in the structure of either site. .
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