In the R5 - ZFN control group, with intact cxcr4 genes, 88 % of CD4 + T
cells expressed CXCR4 protein at day 27 post engraftment, compared to 84 % of cells in the X4 - ZFN mice (∼ 24 % cxcr4 gene disruption) as determined by a fluorescence minus - one (FMO) control.
Following coronary artery occlusion, SDF - 1α level is increased in the infarcted area, resulting in the recruitment of progenitor
cells expressing CXCR4 for post-infarct repair [47].
Not exact matches
To examine this, we transiently
expressed CXCR4Δ18 or wt
CXCR4 as a control in 293T
cells, which have low endogenous
CXCR4 expression.
Our long - term goal, therefore, is to explore the potential to genetically disrupt both ccr5 and
cxcr4 for cell replacement therapies in HIV infected individuals, and in the case of cxcr4 do so in a way that specifically targets CXCR4 on T cells and not the many other cell types on which it is expre
cxcr4 for
cell replacement therapies in HIV infected individuals, and in the case of
cxcr4 do so in a way that specifically targets CXCR4 on T cells and not the many other cell types on which it is expre
cxcr4 do so in a way that specifically targets
CXCR4 on T cells and not the many other cell types on which it is expre
CXCR4 on T
cells and not the many other
cell types on which it is
expressed.
To evaluate coreceptor tropism, a representative Env from the X4 - ZFN mice and the viral innoculum were pseudotyped and used to infect NP2
cell lines
expressing CD4 and either CCR5 or
CXCR4.
As full length Bk132 Env would not pseudotype on an NL43 HIV core we truncated the cytoplasmic tail of the Envs [49], [50], and conducted tropism testing on NP2
cell lines
expressing CD4 with either CCR5 or
CXCR4.
SDF - 1 is predominantly overexpressed in skin and kidney, making them the final destinations of
CXCR4 -
expressing cells.
The parent TZM - bl
cell line is an engineered HeLa
cell clone that
expresses human CD4, CCR5 and
CXCR4 and contains HIV - 1 Tat -
GCSF and hypoxia inducible factor - 1α (HIF - 1α) have been shown to up - regulate SDF - 1α in the infarcted area in a rabbit ischemia model and promote the migration of
CXCR4 expressing cells towards cardiac tissues [47 - 49].
Chronic lymphocytic leukemia B
cells express functional
CXCR4 chemokine receptors that mediate spontaneous migration beneath bone marrow stromal
cells.
The parent TZM - bl
cell line is an engineered HeLa
cell clone that
expresses human CD4, CCR5 and
CXCR4 and contains HIV - 1 T
Human CD4
cell expressing Simian
CXCR4.
The parent TZM - bl
cell line is an engineered HeLa
cell clone that
expresses human CD4, CCR5 and
CXCR4 and contains HIV - 1 Ta
SDF - 1 is
expressed in synovial epithelial
cells and it has been reported that persistent induction of
CXCR4 by stromal derived factors, such as TGF - β led to SDF - 1 mediated accumulation of CD4 T
cells within the rheumatoid joint [44].
In addition, the organs and tissues that possess high levels of SDF - 1, such as liver, lung, bone marrow, and lymph nodes, attract the migration of
CXCR4 -
expressing cancer
cells [22].
CXCR4, which is a chemokine receptor, is
expressed in migratory and post-migratory germ
cells in vivo in mice [27], and is also a marker for germ
cells derived from human ES
cells [28], thus suggesting that
CXCR4 is a candidate marker gene for detecting ES
cells - derived germ
cell in monkeys.