Sentences with phrase «+ cells gene»

In my previous reports I excluded some trials, which could fit definition of ATMP (for example, CD34 + cells gene - modified ex vivo or cord blood cells expanded / stimulated ex vivo), now we have included them.

Not exact matches

This is how progesterone boosts CK5 + cells — like tiny gatekeepers, progesterone receptors and their cofactors sit in front of the gene CK5, opening the doors of DNA to be read at this point.

Although that marker, called IL21, had not previously been associated with autoimmune diseases, the gene that produces it sits right in the stretch of DNA known to make these mice vulnerable to diabetes, suggesting that IL21 might make a drug target, says Sarvetnick.Furthermore, by giving the animals a shot of dead bacteria — similar to an immunization in humans — when they were newborns, Sarvetnick and her colleagues prevented a surfeit of CD4 + and CD8 + cells.

The team reports that the adenomas grow from cells that express a gene called Lgr5 +, which is also active in normal intestinal stem cells.

With chronically infected mice as their model, the researchers used a new technology called ATAC - seq to map the regulatory regions of the genome — the sections of DNA involved in switching genes on and off — in the animals» exhausted and functional CD8 + T cells.

The drug, lapatinib, activates the suppressor called FOXO, in HER2 + breast cancer cells, but then FOXO becomes a turncoat molecule, working with an epigenetic regulator that controls gene expression.

Single - cell differential gene expression analysis revealed a spectrum of known transcripts, including several linked to cytotoxic and costimulatory function that are expressed at higher levels in the TEMRA (effector memory T cells expressing CD45RA) subset, which is highly enriched for CD4 - CTLs, compared with CD4 + T cells in the central memory (TCM) and effector memory (TEM) subsets.

Subsequent RNA sequencing suggested that digoxin inhibits HIV - 1 gene expression as well as the activation and metabolism of CD4 + T cells.

Further analysis showed that wild type HIV - 1 tends to integrate itself into or near genes affecting CD4 + T cell activation and metabolism more frequently than does the mutant strain.

In this paper, we report that HIV - 1 prefers to integrate into o near genes that control such changes in CD4 + T cells so that the virus is better able to remain coupled to the CD4 + T cell status.

They also show increased expression of the estrogen receptor alpha [ER +] gene that drives cell division,» says Koshy.

Using bioinformatics tools to identify and map out specific components and regulatory interconnections, the study team found highly dynamic activities during CD8 + T cell responses: a distinct repertoire of super enhancers — groups of enhancers that interact with promoters to drive gene transcription, new groups of enhancers that jump into activity only in the memory cell stage, and extensive re-wiring of regulatory circuits from one cell stage to another.

Moreover, the gene expression responses in CD4 + T cells stimulated with WNV differed between individuals with previous asymptomatic infection and those who had neuro - invasive WNV disease.

The three stages of CD8 + T cell development are well known, but the current study identifies a detailed map of the regulatory circuitry, such as interactions between enhancers and promoters — genetic regulatory regions that function together in driving genes to transcribe proteins to carry out biological processes.

After preclinical studies, a gene therapy trial for SCID - X1 was initiated, based on the use of complementary DNA containing a defective γc Moloney retrovirus — derived vector and ex vivo infection of CD34 + cells.

The new findings, published online in the journal Molecular Cancer Therapeutics, show that combining rapamycin with a gene therapy approach enhanced the animals» ability to summon immune cells called CD8 + T cells to kill tumor cells directly.

Professor Haase also studies the relevance of genetic polymorphisms of DNA - repair and detoxification genes for AML and MDS, the relevance of iron overload for stem cell functions in MDS, and the establishment of FISH analysis of CD34 + cells from the peripheral blood as a diagnostic tool for screening and monitoring in patients with MDS.

Following introduction into human CD4 + T cells [23] or hematopoietic stem cells [28] via an adenovirus vector or DNA nucleofection, respectively, the ccr5 gene was efficiently and specifically disrupted.

Among the three isolated cell populations, the relative gene expression of macrophage markers was highest among the F4 / 80 + cells.

Similar to latently infected CD4 + T cells, the J - Lat cells harbor a full - length HIV - 1 genome that is transcriptionally competent, is integrated within actively transcribed cellular genes, and is inhibited at the transcriptional level.

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.

(B, C) Flow cytometric analysis of HIV - 1 gene expression in (B) mock infected or (C) latently infected CD4 + T cells under non-polarizing conditions, either at the basal state or after reactivation with antibodies against CD3 and CD28.

F4 / 80 + and F4 / 80 — cells were collected into cooled FACS buffer, centrifuged at 500 g for 5 minutes, and immediately frozen for gene expression analysis.

However, coreceptor - specific ZFNs represent a novel therapeutic approach to recapitulate this success via autologous transplantation of gene - modified hematopoietic stem cells and mature CD4 + T cells.

Han et al. demonstrated that in Caco2 cells, extracellular NAD + inhibited the binding of NF - kB to DNA by blocking the transcription of different genes involved in both inflammatory and aging pathways (interlukin - 6, interlukin - 1 beta, tumor necrosis factor alpha) 27.

Glucose deprivation inhibits multiple key gene expression events and effector functions in CD8 + T cells.

These results suggest that inhibition of mTOR - raptor complex or silencing mTOR gene expression induced cell cycle arrest at G1 phase in ALK + ALCL cells.

Targeted Gene Addition to a Safe Harbor locus in human CD34 + Hematopoietic Stem Cells for Correction of X-linked Chronic Granulomatous Disease.

We also show that inhibition of mTOR with rapamycin, as well as silencing mTOR gene product expression using mTOR - specific small interfering RNA, decreased phosphorylation of mTOR signaling proteins and induced cell cycle arrest and apoptosis in ALK + ALCL cells.

Lentiviral - based gene therapy methods to modify human CD34 + hematopoietic stem cells have been investigated as a way of treating various hematological disorders including X-linked chronic granulomatous disease (X-CGD).

Therapeutic levels of fetal hemoglobin in erythroid progeny of -LCB- beta -RCB-- thalassemic CD34 + cells following lentiviral vector - mediated gene transfer.

In addition, an mRNA vaccine encoding the prM and E genes of a French Polynesian strain induced strong CD4 + T cell and neutralizing Ab responses in nonpregnant mice and protected mice and NHPs from virus challenge (118).

In addition to inhibiting STAT5 signaling, we found that depletion of ABL kinases decreased the expression of the Hippo pathway mediator TAZ and downstream target genes in triple - negative and HER2 + breast cancer cells.

While this group of genes is not large, what became apparent from inspection of the heat map in Figure 4A is that the majority of genes upregulated in the V+S − cells are also marginally upregulated when the V − S + to V+S + fractions are compared.

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Most of these genes were significantly down - regulated in both V + fractions and remain high in the V − S − fraction, indicating that this fraction contained a significant proportion of undifferentiated ES cells.

Another group investigated CD8 + T cells, and found that babies had epigenetic and gene expression profiles that resembled those of innate immune cells, which «may provide a partial explanation for infants» higher susceptibility to infectious pathogens,» GenomeWeb reported.

We found that the V+S + population expressed sets of genes that fell into major functional categories that were associated with «Cell adhesion» and «Cell migration.»

In addition to expressing slightly increased PrEn gene expression, V+S + cells also contain almost all the phospho - ERK activity in our ES cell cultures (Figure 6).

Moreover, in PrEn precursors, the Nanog low population can itself be split based on the expression of Oct4 or SSEA - 1 into a state expressing reasonably high level of PrEn genes (V+S −), and a less differentiated cell type exhibiting a PrEn bias, but with similar regenerative capacities to the Nanog high population (V+S +).

Abbreviations: Aβ, amyloid β - peptide; AD, Alzheimer's disease; ALS, amyotrophic lateral sclerosis; Ambra1, activating molecule in Beclin -1-regulated autophagy; AMPK, AMP - activated protein kinase; APP, amyloid precursor protein; AR, androgen receptor; Atg, autophagy - related; AV, autophagic vacuole; Bcl, B - cell lymphoma; BH3, Bcl - 2 homology 3; CaMKKβ, Ca2 + - dependent protein kinase kinase β; CHMP2B, charged multivesicular body protein 2B; CMA, chaperone - mediated autophagy; 2 ′ 5 ′ ddA, 2 ′, 5 ′ - dideoxyadenosine; deptor, DEP - domain containing mTOR - interacting protein; DRPLA, dentatorubral pallidoluysian atrophy; 4E - BP1, translation initiation factor 4E - binding protein - 1; Epac, exchange protein directly activated by cAMP; ER, endoplasmic reticulum; ERK1 / 2, extracellular - signal - regulated kinase 1/2; ESCRT, endosomal sorting complex required for transport; FAD, familial AD; FDA, U.S. Food and Drug Administration; FIP200, focal adhesion kinase family - interacting protein of 200 kDa; FoxO3, forkhead box O3; FTD, frontotemporal dementia; FTD3, FTD linked to chromosome 3; GAP, GTPase - activating protein; GR, guanidine retinoid; GSK3, glycogen synthase kinase 3; HD, Huntington's disease; hiPSC, human induced pluripotent stem cell; hVps, mammalian vacuolar protein sorting homologue; IKK, inhibitor of nuclear factor κB kinase; IMPase, inositol monophosphatase; IP3R, Ins (1,4,5) P3 receptor; I1R, imidazoline - 1 receptor; JNK1, c - Jun N - terminal kinase 1; LC3, light chain 3; LD, Lafora disease; L - NAME, NG - nitro - L - arginine methyl ester; LRRK2, leucine - rich repeat kinase 2; MIPS, myo - inositol -1-phosphate synthase; mLST8, mammalian lethal with SEC13 protein 8; MND, motor neuron disease; mTOR, mammalian target of rapamycin; mTORC, mTOR complex; MVB, multivesicular body; NAC, N - acetylcysteine; NBR1, neighbour of BRCA1 gene 1; NOS, nitric oxide synthase; p70S6K, ribosomal protein S6 kinase - 1; PD, Parkinson's disease; PDK1, phosphoinositide - dependent kinase 1; PE, phosphatidylethanolamine; PI3K, phosphoinositide 3 - kinase; PI3KC1a, class Ia PI3K; PI3KC3, class III PI3K; PI3KK, PI3K - related protein kinase; PINK1, PTEN - induced kinase 1; PKA, protein kinase A; PLC, phospholipase C; polyQ, polyglutamine; PS, presenilin; PTEN, phosphatase and tensin homologue deleted from chromosome 10; Rag, Ras - related GTP - binding protein; raptor, regulatory - associated protein of mTOR; Rheb, Ras homologue enriched in brain; rictor, rapamycin - insensitive companion of mTOR; SBMA, spinobulbar muscular atrophy; SCA, spinocerebellar ataxia; SLC, solute carrier; SMER, small - molecule enhancer of rapamycin; SMIR, small - molecule inhibitor of rapamycin; SNARE, N - ethylmaleimide - sensitive factor - attachment protein receptor; SOD1, copper / zinc superoxide dismutase 1; TFEB, transcription factor EB; TOR, target of rapamycin; TSC, tuberous sclerosis complex; ULK1, UNC -51-like kinase 1; UVRAG, UV irradiation resistance - associated gene; VAMP, vesicle - associated membrane protein; v - ATPase, vacuolar H + - ATPase; Vps, vacuolar protein sorting

Our observation that the V+S + fraction preferentially contributes to the VE when mixed with more ICM - like cells indicates that low - level lineage - specific changes in gene expression have functional consequences.

Independent, spontaneous mutants of adenovirus type 2 - simian virus 40 hybrid Ad2 + ND3 that grow efficiently in monkey cells possess indentical mutations in the adenovirus type 2 DNA - binding protein gene

It is not just stem cell research that is misguided; it is that generally cell research and life research are misguided \ n \ nI humbly suggest, again and again: \ n \ n «Genostemness Induction, More On The Lifehood Of Genes», that makes each and all organisms alive \ n \ nhttps: / / www.the-scientist.com/community/posts/list/160/122.page\n\n\nDov Henis \ n (Comments From The 22nd Century) \ nUpdated Life's Manifest May 2009 \ nhttps: / / www.the-scientist.com/community/posts/list/140/122.page#2321\nImplications Of E = Total [m (1 + D)-RSB- \ nhttps: / / www.the-scientist.com/community/posts/list/180/122.page#310 8

Results: Within 4 h, activation of CD4 (+) T cells invokes changes in histone modifications and enhancer RNA transcription that correspond to altered expression of the interacting genes identified by promoter capture Hi - C.

Unbiased clustering analysis of P (+) neurons revealed four different classes, each with distinct cell surface receptor gene expression profiles.

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Genes putatively related to calcification (e.g. calcium and inorganic carbon transport, H + transport and carbonic anhydrases) have been identified via gene expression studies comparing calcifying and non-calcifying E. huxleyi cells [25 — 29], or in short - term experiments where calcification was regulated by limitation of ions needed for calcification (i.e. Ca2 +, HCO3 − / CO32 − [26,30,31]-RRB-.