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Foot-and-mouth disease virus VP1 as an interferon-suppressor by interacting with sorcin.
Sorcin is able to limit the toxic effects of the chemotherapeutic agent in the cell. In addition, Sorcin silencing increases cell death upon treatment with doxorubicin, increases the accumulation of doxorubicin in cell nucleus, decreases the expression of MDR1 and doxorubicin efflux via MDR1.
Sorcin overexpression in HCT116 cells resulted in a significant increase in cell migration and invasion. Sorcin stimulated epithelial-mesenchymal transition through activating PI3K/Akt signaling.
The authors verified that NS5A of hepatitis C virus interacted with sorcin through domain I of NS5A, and phosphorylation of the threonine residue 155 of sorcin played a crucial role in protein interaction.
Drug resistance can be effectively reversed in cisplatin-resistance and adriamycin-resistant myeloma cells through delivery of siRNAs targeting sorcin.
Sorcin is highly expressed in the heart and in the brain, and overexpressed in many cancer cells. [Review]
Sorcin antibody as a possible predictive factor in conversion from radiologically isolated syndrome to multiple sclerosis: a preliminary study
Sorcin links calcium signaling to vesicle trafficking, regulates Polo-like kinase 1 and is necessary for mitosis.
Key cellular signaling pathways were triggered by sorcin silencing in the drug resistance of human nasopharyngeal carcinoma.
sorcin regulates epithelial-mesenchymal transition and cancer stem cells partly through E-cadherin and vascular endothelial growth factor expression.
overexpression of sorcin increased the phosphorylation of CREB1 and the binding of CREB1 to the CRE sequence of mdr1/p-gp promoter, and induced the expression of MDR1/P-gp
down-regulation of sorcin did not alter expression or function of P-gp, but induced cell apoptosis and chemosensitivity in K562/ A02 and MCF-7/A02
The role of sorcin in multidrug resistance in cancer. [Review]
sorcin retains ChREBP in the cytosol at low glucose concentrations and may act as a Ca(2+) sensor for glucose-induced nuclear translocation and the activation of ChREBP-dependent genes.
Data show that colorectal cancer cells overexpress sorcin as an adaptive mechanism to prevent endoplasmic reticulum stress and escape apoptosis triggered by chemotherapeutic agents.
Upregulation of sorcin is associated with gastric cancer.
Overexpression of sorcin by gene transfection was able to confer drug resistance in gastric cancer cells
Overexpression of sorcin was associated with gemcitabine resistance in non-small cell lung cancer.
The study indicates that stomatin, sorcin, and synexin are echinophilic membrane components that mainly locate outside GM1 rafts in the human erythrocyte membrane.
Depletion of TRAP1 by short hairpin RNA in colorectal carcinoma cells lowered Sorcin levels in mitochondria, whereas the depletion of Sorcin by small interfering RNA increased TRAP1 degradation.
Overexpression of sorcin could induce low level of multidrug resistant (MDR) in SGC7901 cells, indicating that sorcin is associated with MDR of SGC7901 cells.
Sorcin links pancreatic beta cells lipotoxicity to calcium stores and provides a target for intervention in type 2 diabetes.
Regulation of calcium signaling and cardiac contractility by miR-1 regulated sorcin expression plays a fundamental role in the maintenance of normal cardiac function and in the pathogenesis of cardiac dysfunction.
sorcin is a potent inhibitor of both spontaneous and ICa-triggered RyR activity and is kinetically capable of playing a role in terminating the positive feedback loop of Ca2+-induced Ca2+ release
Data further define the role of sorcin in cardiac excitation-contraction coupling and highlight its negative regulation of sarcoplasmic reticulum calcium release.
Interaction of calcium/calmodulin-dependent protein kinase IIdeltaC with sorcin indirectly modulates ryanodine receptor function in cardiac myocytes.
This gene encodes a calcium-binding protein with multiple E-F hand domains that relocates from the cytoplasm to the sarcoplasmic reticulum in response to elevated calcium levels. In addition to regulating intracellular calcium homeostasis it also modulates excitation-contraction coupling in the heart. Alternative splicing results in multiple transcript variants encoding distinct proteins. Multiple pseudogenes exist for this gene.
, 22 kDa protein
, calcium binding protein amplified in mutlidrug-resistant cells