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HeLa COL1G610C transfected cells; RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Rattus norvegicus Homo sapiens

PROVIDER: GSE239528 | GEO | 2024/06/11

REPOSITORIES: GEO

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HeLa COL1G610C transfected cells RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C

Project description:HeLa COL1G610C transfected cells RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C

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Transcriptome profile of RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C compared to control

Project description:To analyse gene expression differences between RCS COL2R789C transfected cells WT and TFEB/3 DKO compared to their relative scramble controls

2024-06-11 | GSE239527 | GEO

Transcriptome profile of RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C compared to control

Project description:Transcriptome profile of RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C compared to control

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Transcriptome analysis of control and TFEB/TFE3 DKO MEFs and RAW264.7 in response to DNA Damage

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-09-30 | GSE118518 | GEO

Functional genomic analysis of WT, Tet1-/-, Tet2-/-, Tet1-/-:Tet2-/- (DKO) murine embryonic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Metabolic inhibition increases activity of connexin-32 hemichannels permeable to Ca2+ in transfected HeLa cells.

Project description:Numerous cell types express functional connexin (Cx) hemichannels (HCs), and membrane depolarization and/or exposure to a divalent cation-free bathing solution (DCFS) have been shown to promote HC opening. However, little is known about conditions that can promote HC opening in the absence of strong depolarization and when extracellular divalent cation concentrations remain at physiological levels. Here the effects of metabolic inhibition (MI), an in vitro model of ischemia, on the activity of mouse Cx32 HCs were examined. In HeLa cells stably transfected with mouse Cx32 (HeLa-Cx32), MI induced an increase in cellular permeability to ethidium (Etd). The increase in Etd uptake was directly related to an increase in levels of Cx32 HCs present at the cell surface. Moreover, MI increased membrane currents in HeLa-Cx32 cells. Underlying these currents were channels exhibiting a unitary conductance of approximately 90 pS, consistent with Cx32 HCs. These currents and Etd uptake were blocked by HC inhibitors. The increase in Cx32 HC activity was preceded by a rapid reduction in mitochondrial membrane potential and a rise in free intracellular Ca(2+) concentration ([Ca(2+)](i)). The increase in free [Ca(2+)](i) was prevented by HC blockade or exposure to extracellular DCFS and was virtually absent in parental HeLa cells. Moreover, inhibition of Cx32 HCs expressed by HeLa cells in low-confluence cultures drastically reduced cell death induced by oxygen-glucose deprivation, which is a more physiological model of ischemia-reperfusion. Thus HC blockade could reduce the increase in free [Ca(2+)](i) and cell death induced by ischemia-like conditions in cells expressing Cx32 HCs.

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Gene expression analysis and DNA methylation profiling in WT-AG-haESCs, DKO-AG-haESCs and round spermatids

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-06-29 | E-GEOD-60076 | biostudies-arrayexpress

TFEB in HEK293 cells by TET-OFF system (HEK293-PFL-TFEB).

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-28 | GSE98248 | GEO

Wild-type and mutant ferroportins do not form oligomers in transfected cells.

Project description:Ferroportin [FPN; Slc40a1 (solute carrier family 40, member 1)] is a transmembrane iron export protein expressed in macrophages and duodenal enterocytes. Heterozygous mutations in the FPN gene result in an autosomal dominant form of iron overload disorder, type-4 haemochromatosis. FPN mutants either have a normal iron export activity but have lost their ability to bind hepcidin, or are defective in their iron export function. The mutant protein has been suggested to act as a dominant negative over the wt (wild-type) protein by multimer formation. Using transiently transfected human epithelial cell lines expressing mouse FPN modified by the addition of a haemagglutinin or c-Myc epitope at the C-terminus, we show that the wtFPN is found at the plasma membrane and in Rab5-containing endosomes, as are the D157G and Q182H mutants. However, the delV162 mutant is mostly intracellular in HK2 cells (human kidney-2 cells) and partially addressed at the cell surface in HEK-293 cells (human embryonic kidney 293 cells). In both cell types, it is partially associated with the endoplasmic reticulum and with Rab5-positive vesicles. However, this mutant is complex-glycosylated like the wt protein. D157G and G323V mutants have a defective iron export capacity as judged by their inability to deplete the intracellular ferritin content, whereas Q182H and delV162 have normal iron export function and probably have lost their capacity to bind hepcidin. In co-transfection experiments, the delV162 mutant does not co-localize with the wtFPN, does not prevent its normal targeting to the plasma membrane and cannot be immunoprecipitated in the same complex, arguing against the formation of FPN hetero-oligomers.

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Chromatin immunoprecipitation and expression analysis in WT and hrr25 mutant cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-12-02 | GSE107166 | GEO