Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

ABSTRACT: We report differentially expressed genes as a result of activation of L-type calcium channel CaV1.2 with GOF mutation in mVICs.

ORGANISM(S): Mus musculus

PROVIDER: GSE151520 | GEO | 2021/06/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

Project description:DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

| PRJNA636195 | ENA

Quality control at the cell surface prevents accumulation of damaged L-type CaV1.2 calcium channels

Project description:Defective ion channel turnover and clearance of damaged proteins are associated with aging and neurodegeneration. The L-type CaV1.2 voltage-gated calcium channel mediate depolarization-induced calcium signals in heart and brain. Here, we determined the interaction surface between the L-type calcium channel CaVβ subunit and actin using cross-linking mass spectrometry and protein-protein docking, and uncovered a role in replenishing damaged CaV1.2 channels. Computational and in vitro mutagenesis identified hotspots in CaVβ that decrease its affinity for actin but not for CaV1.2. Coexpression of an actin-association-deficient CaVβ mutant with the CaV1.2 channel downregulated current amplitudes with a concomitant reduction in the number of functionally available channels. Neither alterations in the single-channel properties nor changes in the total number of channels at the cell surface were found, indicating that current inhibition resulted from a build-up of conduction-defective channels. Our findings established CaVβ–actin interaction as a key player for selective monitoring and clearing corrupted CaV proteins to ensure the maintenance of a functional pool of channels and proper calcium signal transduction. The CaVβ–actin molecular model introduces a potentially druggable protein-protein interface to intervene CaV-mediated signaling processes.

2024-02-16 | PXD044630 | Pride

Quality control at the cell surface prevents accumulation of damaged L-type CaV1.2 calcium channels

2024-02-16 | PXD044723 | Pride

Leukemic Cells Hijack Stromal Bioelectricity to Reprogram the Bone Marrow Niche via CaV1.2-Dependent Mechanisms

Project description:Mesenchymal stromal cells (MSCs) are key components of the tumor microenvironment (TME), influencing leukemia progression through poorly understood mechanisms. Here, the bioelectrical properties of MSCs derived from pediatric acute myeloid leukemia (AML) patients (AML-MSCs) are investigated, identifying a significant depolarization of their resting voltage membrane potential (Vmem, -14.7 mV) compared to healthy MSCs (h-MSCs, -28.5 mV), accompanied by downregulation of Calcium channel, voltage-dependent, L type, alpha 1C subunit1.2 (CaV1.2) L-type calcium channel expression. AML-MSCs display increased spontaneous calcium oscillations, suggesting altered ion homeostasis. Notably, h-MSCs exposed to AML blasts undergo a similar Vmem depolarization (-11.8 mV) and CaV1.2 downregulation, indicating that leukemic cells actively reprogram MSCs. Functionally, Vmem depolarization in h-MSCs promotes a pro-leukemic phenotype, whereas hyperpolarization of AML-MSCs restores a normal behavior. CaV1.2 over-expression by lentiviral vectors in AML-MSCs shifts the Vmem toward hyperpolarization and partially reverses their leukemia-supportive properties, in part through CaV1.2 transfer via tunneling nanotubes. These findings reveal that AML blasts impose a bioelectrical signature on MSCs, modulating ion channel activity to sustain a leukemic niche. Targeting this electrical reprogramming through CaV1.2 restoration represents a potential strategy to re-establish homeostasis in the bone marrow microenvironment.

2025-11-28 | GSE248681 | GEO