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Store-Independent Calcium Entry and Related Signaling Pathways in Breast Cancer
Known as a key effector in breast cancer (BC) progression, calcium (Ca(2+)) is tightly regulated to maintain the desired concentration to fine-tune cell functions. Ca(2+) channels are the main actors among Ca(2+) transporters that control the intracellular Ca(2+) concentration in cells. It is well k...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8303984/ https://www.ncbi.nlm.nih.gov/pubmed/34209733 http://dx.doi.org/10.3390/genes12070994 |
Sumario: | Known as a key effector in breast cancer (BC) progression, calcium (Ca(2+)) is tightly regulated to maintain the desired concentration to fine-tune cell functions. Ca(2+) channels are the main actors among Ca(2+) transporters that control the intracellular Ca(2+) concentration in cells. It is well known that the basal Ca(2+) concentration is regulated by both store-dependent and independent Ca(2+) channels in BC development and progression. However, most of the literature has reported the role of store-dependent Ca(2+) entry, and only a few studies are focusing on store-independent Ca(2+) entry (SICE). In this review, we aim to summarize all findings on SICE in the BC progression field. |
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