ArticlePloS one2015
Regulation of L-type Voltage Gated Calcium Channel CACNA1S in Macrophages upon Mycobacterium tuberculosis Infection.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- The host susceptibility/resistance-related genes and gut microbial characteristics inMicrobiology spectrum · 2025Article
- Toll-like receptor adaptor protein TIRAP has specialized roles in signaling, metabolic control and leukocyte migration upon wounding in zebrafish larvae.International journal of biological sciences · 2025Article
- Aflatoxin B1 affects porcine alveolar macrophage growth through the calcium signaling pathway mediated by the ceRNA regulatory network.Molecular biology reports · 2023Article
- Electrical stimulation of cochlear implant promotes activation of macrophages and fibroblasts under inflammation.Laryngoscope investigative otolaryngology · 2023Article
- The contribution of ion channels to shaping macrophage behaviour.Frontiers in pharmacology · 2022Review
- CACNA1S haploinsufficiency confers resistance to New World arenavirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages.BioMed research international · 2020Article
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- Role of STIM2 in cell function and physiopathology.The Journal of physiology · 2017Review
- Genome-wide association study for acute otitis media in children identifies FNDC1 as disease contributing gene.Nature communications · 2016Article
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- Igf1 and Pacap rescue cerebellar granule neurons from apoptosis via a common transcriptional program.Cell death discoveryArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We demonstrated earlier the inhibitory role played by Voltage Gated Calcium Channels (VGCCs) in regulating Mycobacterium tuberculosis (M. tb) survival and pathogenesis. In this report, we investigated mechanisms and key players that regulate the surface expression of VGCC-CACNA1S by Rv2463 and M. tb infection in macrophages. Our earlier work identified Rv2463 to be expressed at early times post infection in macrophages that induced suppressor responses to dendritic cells and macrophages. Our results in this study demonstrate a role of MyD88 independent TLR pathway in mediating CACNA1S expression. Dissecting the role for second messengers, we show that calcium homeostasis plays a key role in CACNA1S expression during M. tb infection. Using siRNAs against molecular sensors of calcium regulation, we show an involvement of ER associated Stromal Interaction Molecules 1 and 2 (STIM1 and STIM2), and transcription factor pCREB, towards CACNA1S expression that also involved the MyD88 independent pathway. Interestingly, reactive oxygen species played a negative role in M. tb mediated CACNA1S expression. Further, a cross-regulation of ROS and pCREB was noted that governed CACNA1S expression. Characterizing the mechanisms governing CACNA1S expression would improve our understanding of the regulation of VGCC expression and its role in M. tb pathogenesis during M. tb infection.
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