- PA5-23740 - Invitrogen Antibodies CAMK2N1 antibody

Submitted references MiR-129-5p promotes docetaxel resistance in prostate cancer by down-regulating CAMK2N1 expression.

Wu C, Miao C, Tang Q, Zhou X, Xi P, Chang P, Hua L, Ni H
Journal of cellular and molecular medicine 2020 Feb;24(3):2098-2108

SYT12 plays a critical role in oral cancer and may be a novel therapeutic target.

Eizuka K, Nakashima D, Oka N, Wagai S, Takahara T, Saito T, Koike K, Kasamatsu A, Shiiba M, Tanzawa H, Uzawa K
Journal of Cancer 2019;10(20):4913-4920

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot analysis using a CAMK2N1 polyclonal antibody (Product # PA5-23740) in mouse testis tissue lysates (35 µg per lane).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 3 Involvement of the SYT12 signaling pathways that mediate the migratory and invasiveness phenotype of OSCCs. (A) Migration assay of shMock cells and shSYT12 cells (N=3). (B) Invasion assay of shMock cells and shSYT12 cells at 24h (N=3). (C) Immunoblot analysis shows CAMK2N1 expression is increased in the shSYT12 cells, CAMK2 expression is similar in the shMock cells and shSYT12, but phosphorylation of CAMK2 (p-CAMK2) is decreased in the shSYT12 cells compared with the shMock cells (N=3).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 1 Differential expression of CAMK 2N1 in prostate cancer resistant cell lines. (A) Heat map of differentially expressed mRNA s in normal and docetaxel-resistant ( DR ) cell lines ( DU -145 and PC -3). The colour gradation indicates the log of fold change ( FC ) with a base of 2. (B) The relative mRNA expression levels of CAMK 2N1 in 18 pairs of docetaxel-free and DR tissues of prostate cancer patients were detected by qRT - PCR . Data are expressed as mean +- SD (n = 36). * P < 0.05 compared to the docetaxel-free group. (C, D) The relative mRNA and protein expression levels of CAMK 2N1 in prostate cancer cell line PC -3 and PC -3 DR cell line ( PC -3- DR ) were detected by qRT - PCR and western blot. Data are expressed as mean +- SD (n = 36). ** P < 0.01 compared to the PC-3 group

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 3 CAMK 2N1 inhibited docetaxel resistance in prostate cancer ( PC a). (A, B) After CAMK 2N1 overexpression vector (pc DNA 3.1- CAMK 2N1 ) transfection, CAMK 2N1 mRNA expression was determined by qRT - PCR and western blot in PC -3- DR cells. Data are expressed as mean +- SD (n = 4). ** P < 0.01 compared to the control group. (C) Cell survival rate of PC -3- DR treated with DTX was detected by CCK -8 assay at days 0, 1, 2, 3, 4 and 5, respectively. (D) Apoptotic cell death was measured with flow cytometry analyses after transfection with pc DNA 3.1- CAMK 2N1 and treatment of DTX for 24 h. * P < 0.05, ** P < 0.01, *** P < 0.001. (E, F) PC a cells invasion and migration ability were detected after treatment of DTX for 24 h, scale bar = 50 mum. The cell numbers were counted and results are expressed as mean +- SD (n = 5). ** P < 0.01 compared to the PC -3 group

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 MiR-129-5p promoted the drug resistance of docetaxel in PC a by targeting CAMK 2N1 . (A) miR-129-5p mimics and inhibitors expressed in PC -3- DR cells. Data are expressed as mean +- SD (n = 4). ** P < 0.01 compared to the control group. (B) Effects of miR-129-5p mimics and inhibitors on CAMK 2N1 mRNA was detected by qRT - PCR . Data are expressed as mean +- SD (n = 4). ** P < 0.01 compared to the control group. (C) Effects of miR-129-5p mimics and inhibitors on CAMK 2N1 protein was detected by western blot. Data are expressed as mean +- SD (n = 4). ** P < 0.01 compared to the control group. (D) After treated PC -3- DR cell with DTX (60 nmol/L) for 24 h, miR-129-5p promoted cell survival of PC -3- DR while CAMK 2N1 inhibited the positive effect of miR-129-5p on cell survival. * P < 0.05, compared with MOCK + DTX group. (E) MiR-129-5p attenuated apoptosis of PC -3- DR while CAMK 2N1 promoted cell apoptosis. * P < 0.05, ** P < 0.01, compared with MOCK + DTX group; # P < 0.05, compared with mimics+ DTX group. (F, G) MiR-129-5p facilitated the invasion and migration of PC -3- DR while CAMK 2N1 impeded the positive effect of miR-129-5p on cell invasion and migration, scale bar = 50 mum. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with MOCK + DTX group; # P < 0.05, compared with mimics+ DTX group

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 6 CAMK 2N1 reversed the effect of miR-129-5p on inhibiting activation of ERK / MEK and promoting Bax/Bcl2. (A) Expression levels of CAMK 2N1, p- ERK 1/2, ERK 1/2, p- MEK 1, MEK 1, Bcl-2 and BAX were determined by Western blot in PC -3- DR cells. * P < 0.05, ** P < 0.01, compared with MOCK + DTX group; ## P < 0.01, compared with mimics+ DTX group

PA5-23740

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