Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/131847
Title: Sulphate induces very fast cell rounding and detachment
Authors: Sit, K.H. 
Wong, K.P.
Keywords: cell retraction
endocytosis
signal transduction
sodium ion/proton antiport
sulfation
Issue Date: 1991
Citation: Sit, K.H., Wong, K.P. (1991). Sulphate induces very fast cell rounding and detachment. Biochimica et Biophysica Acta - Molecular Cell Research 1092 (2) : 180-183. ScholarBank@NUS Repository.
Abstract: Within a few minutes of incubation with SO4 2-, cultured monolayer cells retract into round shapes with drastically reduced surface area. Concomitant elevation of phosphoinositide second messenger levels, viz, 1,2-diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3), is observed. A causal relationship with sulphation seems to be suggested by finding (a) sulphation of an added acceptor, 4-methylumbelliferone, (b) sulphation of endogenous glycosaminoglycan (GAG) polymers, (c) inhibition by phenol sulphotransferase inhibitor, DCNP (2,6-dichloro-4-nitrophenol). DCNP also inhibits the second messenger production and cell rounding. Reduced surface area appears to be caused by massive plasma membrane internalization in a distinctive endocytosis which is also seen in cell rounding from directly imposed ionic gradients. Reducing the surface area would reduce the adhesive or attachment sites. Besides demonstrating a highly efficient cell detachment potential, huge macromolecules appear to be readily internalized. The association of sulphation, signal transduction and cell detachment is novel.
Source Title: Biochimica et Biophysica Acta - Molecular Cell Research
URI: http://scholarbank.nus.edu.sg/handle/10635/131847
ISSN: 01674889
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

17
checked on Mar 14, 2018

WEB OF SCIENCETM
Citations

14
checked on May 9, 2018

Page view(s)

7
checked on Mar 11, 2018

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.