Science,
Год журнала:
2004,
Номер
304(5678), С. 1800 - 1804
Опубликована: Май 25, 2004
Pathogenic
mycobacteria
resist
lysosomal
delivery
after
uptake
into
macrophages,
allowing
them
to
survive
intracellularly.
We
found
that
the
eukaryotic-like
serine/threonine
protein
kinase
G
from
pathogenic
was
secreted
within
macrophage
phagosomes,
inhibiting
phagosome-lysosome
fusion
and
mediating
intracellular
survival
of
mycobacteria.
Inactivation
by
gene
disruption
or
chemical
inhibition
resulted
in
localization
mycobacterial
cell
death
infected
macrophages.
Besides
identifying
a
target
for
control
infections,
these
findings
suggest
have
evolved
signal
transduction
mechanisms
capable
modulating
host
trafficking
pathways.
Cold Spring Harbor Perspectives in Biology,
Год журнала:
2017,
Номер
10(1), С. a029314 - a029314
Опубликована: Май 15, 2017
Aaron
Buckley
and
Jerrold
R.
Turner
Departments
of
Pathology
Medicine
(Gastroenterology),
Brigham
Women's
Hospital
Harvard
Medical
School,
Boston,
Massachusetts
02115
Correspondence:
jrturner{at}bwh.harvard.edu
Science,
Год журнала:
2004,
Номер
304(5678), С. 1800 - 1804
Опубликована: Май 25, 2004
Pathogenic
mycobacteria
resist
lysosomal
delivery
after
uptake
into
macrophages,
allowing
them
to
survive
intracellularly.
We
found
that
the
eukaryotic-like
serine/threonine
protein
kinase
G
from
pathogenic
was
secreted
within
macrophage
phagosomes,
inhibiting
phagosome-lysosome
fusion
and
mediating
intracellular
survival
of
mycobacteria.
Inactivation
by
gene
disruption
or
chemical
inhibition
resulted
in
localization
mycobacterial
cell
death
infected
macrophages.
Besides
identifying
a
target
for
control
infections,
these
findings
suggest
have
evolved
signal
transduction
mechanisms
capable
modulating
host
trafficking
pathways.