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Fig1: Dot blot analysis of anti-CACNA1C on PVDF. 1ug, 2ug and 4ug of immunization peptides were given in this test. Anti-CACNA1C antibody was diluted with 1/500.
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Fig2: ICC staining CACNA1C in SKOV-3 cells (green). The nuclear counter stain is DAPI (blue). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.
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Fig3: Immunohistochemical analysis of paraffin-embedded rat brain tissue using anti-CACNA1C antibody. Counter stained with hematoxylin.
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Fig4: Immunohistochemical analysis of paraffin-embedded human kidney tissue using anti-CACNA1C antibody. Counter stained with hematoxylin.
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Fig5: Immunohistochemical analysis of paraffin-embedded human uterus tissue using anti-CACNA1C antibody. Counter stained with hematoxylin.
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Fig6: Immunohistochemical analysis of paraffin-embedded mouse heart tissue using anti-CACNA1C antibody. Counter stained with hematoxylin.
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Fig7: Flow cytometric analysis of SKOV-3 cells with CACNA1C antibody at 1/100 dilution (fuchsia) compared with an unlabelled control (cells without incubation with primary antibody; yellow). Alexa Fluor 488-conjugated goat anti-rabbit IgG was used as the secondary antibody.
IHC
B, The protein expression of CACNA1C was negative in one case with rituximab resistance and positive in the other case with rituximab sensitivity, whereas CD20 protein expression was positive in both of them.
WB
A and B, The interference with shRNA to CACNA1C reduced the percentage of rituximab-induced cell apoptosis (P < 0.05) in OCI-ly7 and OCI-Ly8 cell line.
WB
B, CACNA1C protein was detected in anti-CD20 pull-down protein using Western blot after rituximab treatment of 2 hours in OCI-ly7 cells.
WB
D, Proteasome inhibitor bortezomib (20 nmol/L) restored CD20 expression after administration of 6 hours in OCI-ly7 cells.
WB
B, The ectopic expression of miR-363 reduced CACNA1C and CD20 protein expression in OCI-ly7 and OCI-ly8 cell lines.D, The knockout of miR-363 led to the upregulation of CACNA1C expression.