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dictyNews Volume 21 Number 19
Dicty News
Electronic Edition
Volume 21, number 19
December 26, 2003
Please submit abstracts of your papers as soon as they have been
accepted for publication by sending them to dicty@northwestern.edu
or by using the form at
http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit.
Back issues of Dicty-News, the Dicty Reference database and other
useful information is available at dictyBase - http://dictybase.org.
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Abstracts
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Chemotaxis: signalling modules join hands at front and tail
Marten Postma, Leonard Bosgraaf, Harriët M. Loovers, and Peter J.M. Van Haastert
EMBO Reports, Review/Concept
Chemotaxis is the result of a refined interplay between various intracellular
molecules that process spatial and temporal information.
Here we present a modular scheme of the complex interactions between the front
and the back of cells that allows them to navigate. First, at the front of the
cell, activated Rho-type GTPases induce actin polymerization and pseudopod formation.
Second, phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) is produced
in a patch at the leading edge, where it binds PH domain-containing proteins,
which enhance actin polymerization and translocation of the pseudopod.
Third, in Dictyostelium amoebae, a cGMP-signalling cascade has been identified
that regulates myosin filament formation in the posterior of the cell,
thereby inhibiting the formation of lateral pseudopodia that could misdirect the cell.
Submitted by: Peter J.M. Van Haastert [P.J.M.van.Haastert@chem.rug.nl]
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Differentiation-inducing factor-1-induced growth arrest of K562 leukemia cells
involves the reduction of ERK1/2 activity
Emi Akaishi, Torao Narita, Shinjiro Kawai, Yoshikazu Miwa, Toshiyuki Sasaguri,
Kohei Hosaka, Yuzuru Kubohara *
Institute for Molecular and Cellular Regulation (IMCR), Gunma University,
Maebashi 371-8512, Japan
Eur. J. Pharmacol. In press.
Abstract
The differentiation-inducing factor-1 (DIF-1) is a signal molecule that induces
stalk cell differentiation in the cellular slime mold Dictyostelium discoideum.
In addition, DIF-1 is a potent anti-leukemic agent that induces growth arrest in
K562 cells. In this study, we investigated the mechanism of the action of DIF-1
in K562 cells in the light of cell-cycle regulators such as cyclins, retinoblastoma
protein (pRb), and the mitogen-activated protein kinase (MAPK) family.
DIF-1 down-regulated cyclins D/E and a phosphorylated form of pRb (p-pRb) and thereby
induced G1 arrest of the cell cycle. DIF-1 inactivated the extracellular signal-regulated
kinase (ERK) in a bi-phasic manner but did not affect the c-Jun N-terminal kinase (JNK)
or p38 MAPK. The MEK (MAPK kinase) inhibitor, U0126, which has been shown to induce
growth arrest, inactivated ERK and down-regulated cyclins D/E. Although DIF-1
activated the phosphatidylinositol 3-kinase (PI-3K)/Akt pathway, neither wortmannin
nor 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002) (PI-3K inhibitors)
cancelled DIF-1-induced growth arrest. The present results suggest that ERK inactivation
may be involved in DIF-1-induced growth arrest and that PI-3K activity is not required
for DIF-1-induced growth arrest in K562 cells.
Submitted by: Yuzuru Kubohara [kubohara@showa.gunma-u.ac.jp]
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[End Dicty News, volume 21, number 19]
