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Differential Expression of Calcium Channels and Signaling Pathways in Hematologic Cancers

ABSTRACT: Differential Expression of Calcium Channels and Signaling Pathways in Hematologic Cancers

PROVIDER: PRJNA785146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17084908_1.fastq.gz	Fastqsanger.gz
	SRR17084908_2.fastq.gz	Fastqsanger.gz
	SRR17084909_1.fastq.gz	Fastqsanger.gz
	SRR17084909_2.fastq.gz	Fastqsanger.gz
	SRR17084910_1.fastq.gz	Fastqsanger.gz

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Differential Expression of Calcium Channels and Signaling Pathways in Hematologic Cancers

Project description:Cell surface calcium (Ca2+) channels permit Ca2+ ion influx, with Ca2+ taking part in cellular functions such as proliferation, survival, and activation. The expression of voltage-dependent Ca2+ (CaV) channels may modulate the growth of hematologic cancers. Profile analysis of Ca2+ channels, with a focus on the L-type CaV channels, was performed on RNA sequencing data from lymphoma and leukemia cell lines and samples derived from patients with diffuse large B cell lymphoma (DLBCL). CaV1.2 expression was found to be elevated in classical Hodgkin lymphoma (CHL) cell lines when compared to other B cell lymphoma cell lines. In our analysis comparing activated B cell-like DLBCL (ABC-DLBCL) and germinal centre B cell-like DLBCL (GCB-DLBCL) patient samples, ABC-DLBCL revealed stronger expression of CaV1.3, whereas CaV1.1, CaV1.2, and CaV1.4 showed greater expression levels in GCB-DLBCL. As Ca2+ is known to bind to calmodulin, leading to calcineurin activation and the passage of nuclear factor of activated T cells (NFAT) to the cell nucleus, pathways for calcineurin, calmodulin, NFAT, and Ca2+ signaling were also analyzed by gene set enrichment analysis. The NFAT and Ca2+ signaling pathways were found to be upregulated in the CHL cell lines relative to other B cell lymphoma cell lines. Furthermore, the calmodulin and Ca2+ signaling pathways were shown to be downregulated in the ABC-DLBCL patient samples. The findings of this study suggest that L-type CaV channels and Ca2+-related pathways could serve as differentiating components for biologic therapies to target hematological cancers.

2022-06-15 | GSE189927 | GEO

Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events

Project description:Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events

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Static Magnetic Fields Regulate T-Type Calcium Ion Channels and Mediate Mesenchymal Stem Cells Proliferation

Project description:The static magnetic fields (SMFs) impact on biological systems, induce a variety of biological responses, and have been applied to the clinical treatment of diseases. However, the underlying mechanisms remain largely unclear. In this report, by using human mesenchymal stem cells (MSCs) as a model, we investigated the biological effect of SMFs at a molecular and cellular level. We showed that SMF exposure promotes MSC proliferation and activates the expression of transcriptional factors such as FOS (Fos Proto-Oncogene, AP-1 Transcription Factor Subunit) and EGR1 (Early Growth Response 1). In addition, the expression of signal-transduction proteins p-ERK1/2 and p-JNK oscillate periodically with SMF exposure time. Furthermore, we found that the inhibition of the T-type calcium ion channels negates the biological effects of SMFs on MSCs. Together, we revealed that the SMFs regulate T-type calcium ion channels and mediate MSC proliferation via the MAPK signaling pathways.

2022-08-10 | GSE210518 | GEO

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 | PXD044723 | Pride

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

2024-02-16 | PXD044630 | Pride

Microenvironment T-Type calcium channels regulate neuronal and glial processes in glioblastoma

Project description:Microenvironment T-Type calcium channels regulate neuronal and glial processes in glioblastoma

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Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 8 mRNA data]

Project description:Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 8 mRNA data]

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Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 2 mRNA data]

Project description:Co-expression of calcium channels and delayed rectifier potassium channels protects the heart from proarrhythmic events [Figure 2 mRNA data]

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Microenvironment T-Type calcium channels regulate neuronal and glial processes in glioblastoma

Project description:Glioblastoma (GBM) is the most primary common malignant brain tumor. The aim of this study was to elucidate the role of intrinsic and microenvironment T-type calcium channels (Cav3) in promoting tumor growth and progression. Cav3.2 KO in the microenvironment led to significant reduction in GBM growth and prolongation of animal. Single-cell RNA sequencing showed that microenvironment Cav3.2 regulates neuronal and glial biological processes. Microenvironmental Cav3.2 downregulated numerous genes associated with regulating OPC cell state such as SOX10 and Olig2. Neuronal Cav3.2 promoted neuron/GSC synaptic connections and GSC growth. Treatment of GSCs with the Cav3 blocker mibefradil downregulated genes associated with neuronal processes. The combination of mibefradil with temozolomide and radiation significantly reduced tumor volume providing an additive effect compared to TMZ/radiation alone. Together these data reveal a role for microenvironmental Cav3 in promoting GBM tumor progression through regulating neuronal and glial processes particularly associated with the OPC-cell state. Targeting both intrinsic and microenvironment Cav3 with mibefradil significantly enhanced the anti-GBM effects of TMZ and radiation.

2025-07-31 | GSE273629 | GEO

Differential regulation of membrane potential during store-operated calcium entry in neutrophil subsets

Project description:Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2 and ORAI3 are known to comprise the CRAC channel, however the contributions of individual isoforms to neutrophil function is not well understood. Here we show that loss of ORAI1 partially decreases calcium influx while loss of both ORAI1 and ORAI2 completely abolishes store-operated calcium entry. In other immune cell types, loss of ORAI2 enhances SOCE. In contrast, we find that ORAI2-deficient neutrophils display decreased calcium influx, which is correlated with measurable differences in regulation of neutrophil membrane potential via KCa3.1. Decreased SOCE in ORAI1-, ORAI2- and ORAI1/2-deficient neutrophils impairs multiple neutrophil functions including phagocytosis, degranulation, leukotriene and ROS production, rendering ORAI1/2-deficient mice highly susceptible to staphylococcal infection. This study demonstrates that ORAI1 and ORAI2 are the primary components of the neutrophil CRAC channel and identifies novel subpopulations of neutrophils where cell membrane potential functions as a rheostat to modulate the SOCE response. These findings have implications for new mechanisms that modulate neutrophil function during infection, acute and chronic inflammatory conditions, and cancer.

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