Similar Datasets
Project description:Role of GR in FACS sorted CD11B
| PRJNA1370120 | ENA
Project description:Interventions: Share the result of Guardant Reveal test with the patient;ctDNA
Primary outcome(s): This is defined as the percentage of patients whose recommended treatment changed before and after the initial Guardant Reveal test in the FAS. Thisis defined as the percentage of patients for whom the recommended treatment was changed before or after the initial Guardant Reveal test.
A change in recommended therapy is defined as at least one of the following
Addition or deletion of oxaliplatin
Change in the use of postoperative adjuvant therapy
Change in duration of adjuvant therapy.
Study Design: single arm study, open(masking not used), uncontrolled control, single assignment, health services research
| 103018 | ecrin-mdr-crc
Project description:Analyse the impact of GR deletion in macrophages on muscle regeneration at differents time point : 2, 4 and 7 days after injury.
2026-08-21 | GSE311685 | GEO
Project description:Differentially expressed genes of CD11b+Gr-1+ immature myeloid cells (IMCs) in the bone marrow and colonic tumor setting of histidine decarboxylase (HDC)-KO mice were examined by microarray (Affymetrix Mouse 430.2 array). Myeloid differentiation-related candidate genes were sought to be isolated and functionally studied.
2010-12-15 | GSE23502 | GEO
Project description:Differentially expressed genes of CD11b+Gr-1+ immature myeloid cells (IMCs) in the bone marrow and colonic tumor setting of histidine decarboxylase (HDC)-KO mice were examined by microarray (Affymetrix Mouse 430.2 array). Myeloid differentiation-related candidate genes were sought to be isolated and functionally studied. Total RNA of HDC-expressing CD11b+Gr-1+ IMCs of bone marrow were extracted from HDC-EGFP and HDC-EGFP/HDC-KO mice (3 mice in each group). CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) of colon tumor were sorted from 10-12 colon tumors of WT and HDC-KO mice (5 mice in each group), and pooled to extract total RNA for microarray studies. Two technical replicates for each of the four groups. Four sets of comparisons were performed to screen for upregulated or downregulated genes in the HDC-KO CD11b+Gr-1+ IMCs or MDSCs (experiment group) compared to the WT group: (1) HDC-expressing CD11b+Gr-1+ IMCs of bone marrow of HDC KO mice compared to bone marrow IMCs of WT mice; (2) CD11b+Gr-1+ MDSCs in tumors of HDC-KO mice compared to WT mice; (3) CD11b+Gr-1+ MDSCs of WT colon tumors compared to IMCs in the WT bone marrow; and (4) CD11b+Gr-1+ MDSCs of colon tumors of HDC-KO mice compared to IMCs in the bone marrow of HDC-KO mice.
2010-12-15 | E-GEOD-23502 | biostudies-arrayexpress
Project description:Reveal the role of Androgen receptor in satellite cells in muscle regeneration.
2026-08-21 | GSE303614 | GEO
Project description:The Glucocorticoid Receptor (GR) is both one of the most widely used clinical drug targets and a very potent metabolic regulator. GR belongs to the nuclear hormone receptor family of ligand-gated transcription factors that govern mammalian physiology. Upon ligand binding, GR enters the nucleus to regulate gene expression both positively and negatively. It is known to bind to consensus DNA sequences termed glucocorticoid response elements (GREs), but the mechanisms determining transcriptional activation versus repression remain an unresolved molecular paradox. Prevailing models suggest that tethering of GR to AP-1 or NF-κB via protein-protein interactions, rather than direct DNA binding, specifies negative regulation. However, here we show that the repression of inflammatory genes as well as all other glucocorticoid responses, require direct DNA binding of GR. Generating GR point mutant mice that retain the ability to tether via protein-protein interactions while unable to recognize DNA sequences, we demonstrate that response element recognition via the Zinc finger is absolutely required for both transcriptional activation and repression. We have used ChIP-Seq and RNA-Seq in inflammatory and metabolic cells and tissues together with proteomics to reveal that DNA binding of GR is necessary for the assembly of a functional SWI/SNF coregulator complex. Generally, the desired anti-inflammatory actions of GR are attributed to the silencing of inflammatory genes, while its adverse effects are believed to result from the transcriptional upregulation of metabolic targets. Our findings not only challenge classical models and dogmas of GR mediated gene regulation, but will provide an important basis for the development of novel immunosuppressants with reduced side effect profiles.
2020-07-07 | PXD013772 | Pride
Project description:Regeneration of skeletal muscle following injury is accompanied by transient inflammation initiation and resolution. However, it is unclear what signals control these processes. To better understand the biological pathways by C3a-C3aR activation in monocyte druing muscle regeneration,we examined global transcriptional changes in macrophages from the muscle after CTX injury.Male C57BL/6J mice were used at 12 weeks of age. 30 ul 10uM Cardiotoxin (CTX) was injected to TA muscle to injury muscle. CD11b+ cells was isolated from WT and C3aR-/- muscle at 1 day after CTX injury by FACS , then total RNA obtained from these cells were used for the analysis of RNA-seq.
2017-08-31 | E-MTAB-5886 | biostudies-arrayexpress
Project description:FACS sorted glomerular kidney cells from a single mouse were subjected to proteomics.
2022-10-13 | PXD016237 | Pride
Project description:Amyotrophic lateral sclerosis (ALS), the most common form of motor neuron disease, is characterized by progressive muscle weakness and paralysis caused by degeneration of upper and lower motor neurons. A major breakthrough in understanding the genetics of ALS was the discovery of a GGGGCC hexanucleotide repeat expansion (HRE) within the non-coding region of chromosome 9 open reading frame 72 (C9orf72) as the most common mutation in both familial and sporadic forms of ALS [25, 80]. We report that C9orf72 loss of function and poly(GP) expression act together to induce motor neuron degeneration and paralysis. These synergistic properties of C9orf72 mutation affect autophagy, thus resulting in poly(GP) and p62 aggregation. In this context, poly(GP) accumulation occurs in motor neurons preferentially, along with swollen mitochondria, a typical signature of mitophagy defects. In motor neurons, accumulated abnormal mitochondria engage caspase cascade, ultimately giving rise to apoptotic cell death of motor neurons that results in paralysis
2021-05-11 | PXD023967 | Pride