SPARC knock down
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA327124 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparative analysis of the transcriptome of 4T1 cells stably transduced with a lentiviral vector expressing a siRNA against murine SPARC (4T1-C18) with 4T1 control cells stably transduced with a lentiviral vector expressing a scramble sequence (4T1-SCR). Two-condition experiment, 4T1-C18 vs. 4T1-SCR cells. Biological replicates: 4 SPARC knock down, 4 control, independently grown in vitro and harvested. One replicate per array. Microarrays were hybridized in three different days.
2016-06-29 | E-GEOD-83830 | biostudies-arrayexpress
Project description:Comparative analysis of the transcriptome of 4T1 cells stably transduced with a lentiviral vector expressing a siRNA against murine SPARC (4T1-C18) with 4T1 control cells stably transduced with a lentiviral vector expressing a scramble sequence (4T1-SCR).
2016-06-29 | GSE83830 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-06-29 | GSE83832 | GEO
Project description:Fatal neuroendocrine (NE) prostate cancer evolves from castration-resistant adenocarcinoma as a mechanism of resistance to androgen deprivation/anti androgen receptor therapies. Evidence suggests the microenvironment as a possible source of soluble factors mediating neuroendocrine differentiation (NED), but molecular mechanisms are unknown. Using a transgenic mouse model we show that upon castration tumor cells up-regulate GRP78, which triggers a cascade leading to down-regulation of the matricellular protein SPARC in the nearby stroma. SPARC loss allows stroma cells to release IL-6, a known inducer of NED. A drug targeting GRP78 blocks NED in castrated mice. These events find correlation in prostate cancer patients developing focal NED after androgen deprivation therapies. Our results candidate SPARC and GRP78 for diagnostic and therapeutic purpose, respectively.
2021-07-30 | GSE156033 | GEO
Project description:Hyperoxia in FGF10 knock-down mice
| PRJNA306852 | ENA
Project description:Fgf10 knock-down effects in hyperoxia
| PRJNA450016 | ENA
Project description:Fgf10 knock-down effects in normoxia
| PRJNA450017 | ENA
Project description:SPARC is a matricellular glycoprotein involved in regulation of the extracellular matrix, growth factors, adhesion, and migration. SPARC-null mice have altered basement membranes and develop posterior sub-capsular cataracts with cell swelling and equatorial vacuoles. Exchange of fluid, nutrients, and waste products in the avascular lens is driven by a unique circulating ion current. Here we demonstrate that SPARC-null mouse lenses exhibit abnormal circulation of fluid, ion, and small molecules which leads to altered fluorescein distribution in vivo, loss of resting membrane polarization, and altered distribution of small molecules. Microarray analysis of SPARC-null lenses showed changes in gene expression of ion channels and receptors, matrix and adhesion genes, cytoskeleton, immune response genes, and cell signaling molecules. Our results demonstrate that the regulation of SPARC on cell-capsular matrix interactions can influence the circulation of fluid and ions in the lens, and the phenotype in the SPARC-null mouse lens is the result of multiple intersecting pathways. Experiment Overall Design: Lens epithelial cells from 7 lenses of littermate mice were isolated by laser capture microdissection. 3 wild-type lenses from 3 different mice and 4 knock-out lenses from 3 different mice were used as biological replicates.
2009-05-11 | E-GEOD-13402 | biostudies-arrayexpress