Journal: Biochimica et biophysica acta

Article Title: Epoxyeicosatrienoic acids act through TRPV4-TRPC1-KCa1.1 complex to induce smooth muscle membrane hyperpolarization and relaxation in human internal mammary arteries.

doi: 10.1016/j.bbadis.2014.12.010

Figure Lengend Snippet: Fig. 1. Co-immunoprecipitation of TRPV4, TRPC1 and KCa1.1(α) in the lysates of human LIMA VSMCs. A and B, TRPC1 with KCa1.1(α). C and D, TRPC1 with TRPV4. E and F, TRPV4 with KCa1.1(α). The data are representative of 3 to 4 experiments. The pulling antibody and the blotting antibody were indicated (+). Control immunoprecipitation (−) was performed using the preimmune IgG. IP, immunoprecipitation; Blot, immunoblot.

Article Snippet: The primary rabbit antibodies against KCa1.1(α) (APC-021), TRPC1 (ACC-010), and TRPV4 (ACC-034) were from Alomone Labs. T1E3 was raised by us from rabbits.

Techniques: Immunoprecipitation, Control, Western Blot

Journal: Biochimica et biophysica acta

Article Title: Epoxyeicosatrienoic acids act through TRPV4-TRPC1-KCa1.1 complex to induce smooth muscle membrane hyperpolarization and relaxation in human internal mammary arteries.

doi: 10.1016/j.bbadis.2014.12.010

Figure Lengend Snippet: Fig. 5. Membrane potential changes in HEK293 cells that over-expressed with TRPV4, TRPC1 and KCa1.1. A and B, representative traces illustrating the hyperpolarizing responses to 300 nmol/L 11,12-EET (A), 5 μmol/L 4a-PDD (B) and 100 nmol/L GSK1016790A (C). D–F, summary of data showing the maximal hyperpolarization to 300 nmol/L 11,12-EET (D), 5 μmol/L 4a- PDD (E) and 100 nmol/L GSK1016790A (F) under different conditions. C1mut-pore, TRPC1 were replaced by a TRPC1 pore-dead mutant C1mut-pore. Values are means ± SE (n = 5 to 9). **, P b 0.01 compared to the controls (non-transfected); ##, P b 0.01 compared to the transfected cells without inhibitors; $$, P b 0.01 compared to preimmune IgG.

Article Snippet: The primary rabbit antibodies against KCa1.1(α) (APC-021), TRPC1 (ACC-010), and TRPV4 (ACC-034) were from Alomone Labs. T1E3 was raised by us from rabbits.

Techniques: Membrane, Mutagenesis, Transfection

Journal: Biochimica et biophysica acta

Article Title: Epoxyeicosatrienoic acids act through TRPV4-TRPC1-KCa1.1 complex to induce smooth muscle membrane hyperpolarization and relaxation in human internal mammary arteries.

doi: 10.1016/j.bbadis.2014.12.010

Figure Lengend Snippet: Fig. 4. Requirement of TRPC1 for TRPV4 and KCa1.1 interaction. A–D, co-immunoprecipitation of TRPV4 and KCa1.1(α) in the lysates of HEK293 cells. A and B, HEK293 cells that over- expressed with TRPV4, TRPC1 and KCa1.1. C and D, HEK293 cells that over-expressed with TRPV4 and KCa1.1 but without TRPC1. The right lanes in C and D were immunoblots using cell lysates without immunoprecipitation. The pulling antibody and the blotting antibody were indicated (+). Control immunoprecipitation (−) was performed using the preimmune IgG. IP, immunoprecipitation; Blot, immunoblot. n = 3 to 4 experiments. E–F, the maximal hyperpolarization in response to 300 nmol/L 11,12-EET (E) and 5 μmol/L 4α-PDD (F) in HEK293 cells that were transfected with indicated constructs. C1 stands for TRPC1. V4 stands for TRPV4. Values are means ± SE (n = 5 to 9). **P b 0.01 compared to the controls (non-transfected), ##P b 0.01 compared to C1 + V4 + KCa1.1.

Article Snippet: The primary rabbit antibodies against KCa1.1(α) (APC-021), TRPC1 (ACC-010), and TRPV4 (ACC-034) were from Alomone Labs. T1E3 was raised by us from rabbits.

Techniques: Immunoprecipitation, Western Blot, Control, Transfection, Construct

Journal: bioRxiv

Article Title: Cooperative phagocytosis underlies macrophage immunotherapy of solid tumours and initiates a broad anti-tumour IgG response

doi: 10.1101/2022.01.01.474150

Figure Lengend Snippet: Growth curves of mice bearing CD47 KO B16 tumours (2×10 5 s.c. flank injection) and treated i.v. on days 4, 5, 7, 9, 11, 13, and 15 with 250 µg isotype IgG2a control (clone C1.18.4), 100 µl PBS vehicle, or left untreated. Clone C1.18.4 is the isotype control antibody for anti-Tyrp1 clone TA99. There are no significant growth differences (mean ± SEM, n = 6 mice per group).

Article Snippet: Antibodies used for in vivo treatment and blocking, in vitro phagocytosis, flow cytometry, and Western blotting are as follows: anti-mouse/human Tyrp1 clone TA99 (BioXCell BE0151), isotype IgG2a control clone C1.18.4 (BioXCell, BE0085), anti-mouse CD47 clone MIAP301 (BioXCell BE0270), isotype control rat IgG2a (BioXCell, BE0089), anti-mouse SIRPα clone P84 (BioLegend 144004), isotype control rat IgG1 (BioLegend, 400414).

Techniques: Injection, Control

Journal: Cell Research

Article Title: Direct control of store-operated calcium channels by ultrafast laser

doi: 10.1038/s41422-020-00463-9

Figure Lengend Snippet: a Ca 2+ influx intensity of cells treated with 2-APB ( n = 132, 4 trials; n = 129 cells, 5 trials), SKF-96365 ( n = 60, 4 trials; n = 108 cells, 6 trials), YM-58483 ( n = 57, 3 trials; n = 57 cells, 3 trials), and GSK7975A ( n = 60 cells, 3 trials; n = 60 cells, 3 trials) at two different concentrations for a duration of 70 s after the femtoSOC laser illumination. b Add-back test showing Ca 2+ influx suppressed by adding YM-58483 before the femtoSOC laser illumination. Red arrow, timing of the femtoSOC laser illumination. Right, statistics of the measured Ca 2+ influx peak level with or without YM-58483 ( n = 13 cells and n = 17 cells in the control and YM-58483 groups, respectively, P = 0.0061). c Add-back test showing Ca 2+ influx suppressed by adding YM-58483 30 s after the femtoSOC laser illumination. Red arrow, timing of the femtoSOC laser illumination. Orange arrow, timing of the YM-58483 addition. Right, statistics of the Ca 2+ influx decay time defined by the duration of the decay to reach the half maximum of the peak value ( n = 30 cells and n = 24 cells in the control and YM-58483 groups, respectively, P < 0.0001). d Ca 2+ influx probability of cells with Orai1 knockdown ( n = 144 cells, P = 0.0057). Inset, western blot analysis of Orai1 knockdown. e Ca 2+ influx probability of cells with Orai1 overexpression ( n = 135 cells, P = 0.001). Inset, western blot analysis of Orai1 overexpression. f Ca 2+ influx intensity in Orai1/2/3-KO cells compared with that in control cells or that in Orai1/2/3-KO cells with Orai1-mCherry introduced. g No Ca 2+ influx in Orai1-KO cells. h Electrophysiological current of Ca 2+ influx measured by the patch-clamp technique. i Confirmed absence of Zn 2+ and Mg 2+ influx. j Ca 2+ influx probability of cells with TRPC1 knockdown by shRNA ( n = 114 cells, 5 trials, P = 0.3369). Inset, western blot analysis of TRPC1 knockdown. * P < 0.05. ** P < 0.01. *** P < 0.001. **** P < 0.0001. NS, no significant difference. Scale bar, 10 μm.

Article Snippet: Antibodies for immunoblotting were as follows: Orai1 rabbit polyclonal antibody (13130-1-AP, Proteintech, 1:100 dilution), rabbit anti-ORAI1 (O8264, Sigma, 1:1000 dilution), TRPC1 rabbit polyclonal antibody (19482-1-AP, Proteintech, 1:500 dilution), GAPDH mouse monoclonal antibody (60004-1-Ig, Proteintech, 1:10,000 dilution), Peroxidase AffiniPure goat anti-mouse IgG (H + L) (115-035-003, Jackson ImmunoResearch, 1:10,000 dilution), Peroxidase AffiniPure goat anti-rabbit IgG (H + L) (111-035-003, 1:10,000 dilution, Jackson ImmunoResearch).

Techniques: Control, Knockdown, Western Blot, Over Expression, Patch Clamp, shRNA

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 1. Comparison of TRPC expression levels in control and NGF-differentiated PC12 cells. A: Representative bright field images of undifferentiated(control)andNGF-differentiated(NGF)PC12cellsareshown.B:RT-PCRanalysisofTRPCexpressioninPC12cells.PCRproducts amplified using TRPC specific primer sets were separated on ethidium bromide stained agarose gels. A representative gel image is shown. C: Comparison of TRPC expression in control (C) and NGF-differentiated PC12 cells (NGF). Each experiment was repeated 7–9 times.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Comparison, Expressing, Control, Staining

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 2. Western blot analysis of TRPC protein expression in PC12 cells. A: Monoclonal anti-TRPC1 antibody (a generous gift from Dr. Leonidas Tsiokas) was used to detect the TRPC1 protein in control (C) and NGF-differentiated PC12 cells (NGF). The specificity of monoclonal anti-TRPC1 was confirmed using mouse recombinant TRPC proteins. B: TRPC5 protein expression was detected only in undifferentiated PC12 cells. C: NGF pretreatment up-regulated TRPC6 in PC12 cells. In (A)–(C), the lanes labeled mTRPC1, mTRPC5, and hTRPC6 represent recombinant proteins used as controls. ‘‘C’’ denotes control, protein extracts of untreated PC12 cells. ‘‘NGF’’ labels protein extracts isolated from PC12 cells treated with NGF for 48 h. D: Comparison of relative TRPC protein expression levels in control and NGF-differentiated PC12 cells. Each experiment was repeated 10–16 times.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Western Blot, Expressing, Control, Recombinant, Labeling, Isolation, Comparison

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 3. DN-TRPC6 facilitates NGF-induced neurite outgrowth in PC12 cells. A: Comparison of total neurite length per cell in PC12 cells electroporated with a mixture of the YFP plasmid and the pcDNA3 plasmid with or without an insert as indicated. Each group consisted of 35–312 cells. B: Comparison of total neurite length per cell inPC12 cells electroporated with GFP-tagged TRPC constructasindicated. C: Representative images demonstrating the effect of GFP-TRPC6 and DN–GFP–TRPC6 overexpression on the total neurite length per cell. In these pseudocolor images, the red color corresponds to the highest YFP fluorescence, whereas the blue color indicates the lowest YFP fluorescence.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Comparison, Plasmid Preparation, Over Expression

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 5. The effect of hyperforin on neurite outgrowth and TRPC expression in NGF-differentiated PC12 cells. A: Comparison of the total neurite length per cell in hyperforin-treated PC12 cells (n U 405–635). B, C, and D: Hyperforin-induced changes in relative TRPC channel expression in PC12 cells (n U 4 in each group). E: Representative images of gels used during the RT-PCR analysis. HF, hyperforin; Control, undifferentiated PC12 cells; NGF, NGF-differentiated PC12 cells.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Expressing, Comparison, Reverse Transcription Polymerase Chain Reaction, Control

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 4. Electrophysiological characterization of GTPgS-activated currents inTRPC5-overexpressing cells. A: Currents with TRPC5-like current–voltage relationships were observed in the round TRPC5 expressing PC12 cells (n U 8). B: Heteromeric TRPC1–TRPC5 current–voltage relationships were seen in the TRPC5- overexpressing PC12 cells exhibiting neurites (n U 8). The insets in the quadrant II show representative images of TRPC5-expressing PC12 cells, whereas the insets in the quadrant IV show sample current–voltage relationships of the homomeric TRPC5 channel or the TRPC1–TRPC5 heteromeric channel heterologously expressed in HEK cells. The solid line corresponds to the averaged current amplitudes, whereas the vertical bars represent the SEM.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Expressing

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 6. Receptor tyrosine kinase TrkA is not involved in the NGF- induced up-regulation of TRPC1 and TRPC6. A: RT-PCR analysis of TRPC1 (upper panel) and TRPC6 (lower panel) expression in NGF-treated PC12 cells in the absence or presence of 500 nM GW441756, a potent TrkA inhibitor. B: Comparisons of the relative expression levels of TRPC1 and TRPC6 (left, n U 6–7), and the total neurite length per cell (right, n U 276–290) in NGF treated PC12 cells in the absence or presence of 500 nM GW441756.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 7. IKK2 inhibitors abolished NGF-mediated increases of TRPC1 and TRPC6 channel expression in NGF-treated PC12 cells. A: Two different IKK2 inhibitors, BMS (BMS-345541, 10 mM) and IMD (IMD-0354, 1 mM), potently inhibited neurite outgrowth in NGF-differentiated PC12 cells (n U 94–383). B: RT-PCR analysis of TRPC expression in the IKK2 inhibitor treated NGF-differentiated PC12 cells (upper and middle panel). The lower panel shows the effect of the tested IKK2 inhibitors on basal TRPC1 and TRPC5 expression levels in control PC12 cells. TRPC6 expression level was very low in control PC12 cells and was not significantly altered in IKK2 inhibitor experiments (see summary in (C)). Representative gels are shown. C: The summary of RT-PCR analysis of relative TRPC expression in IKK2 inhibitor treated groups. ‘‘NGF R BMS’’ stands for NGF-differentiated PC12 cells treated with (BMS-345541, 10 mM). ‘‘NGF R IMD’’ stands for NGF-differentiated PC12 cells treated with (IMD-0354, 1 mM). ‘‘C’’ denotes undifferentiated PC12 cells. ‘‘NGF’’ denotes NGF differentiated PC12 cells. Each experiment was repeated 4–13 times.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Control

Journal: Journal of cellular physiology

Article Title: Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: the role of TRPC channels.

doi: 10.1002/jcp.22855

Figure Lengend Snippet: Fig. 8. The effect of overexpression of a constitutively active mutant of IKK2 (S177E/S181E, IKK2ca) on TRPC channel expression in PC12 cells. A: IKK2ca-overexpressing undifferentiated PC12 cells exhibited longer neurites than non-transfected cells at 48 h post-electroporation time. Shownisanoverlayofthefluorescenceandcorrespondingbrightfieldimages.TheYFPfluorescenceisshowninpseudo-color.B:Comparisonofthe total neurite length per cell in pcDNA3 and IKK2ca-overexpressing undifferentiated PC12 cells (n U 231–267). C and D: The RT-PCR analysis of TRPC1 and TRPC6 expression in PC12 cells expressing either pcDNA3 or IKK2ca. E, F, and G: The relative changes in the expression of TRPC channels induced by the overexpression of IKK2ca. Each experiment was repeated 10–12 times.

Article Snippet: Conversely, neurite outgrowth was markedly facilitated in NGF-differentiated, TRPC5-defficient PC12 cells overexpressing an shRNA–TRPC5–GFP construct (OriGene, Rockville, MD; Supplemental Fig. 2A–2C) and reduced in NGFdifferentiated, TRPC1-defficient PC12 cells overexpressing shRNA–TRPC1–GFP (OriGene, Rockville, MD; Supplemental Fig. 2D).

Techniques: Over Expression, Mutagenesis, Expressing, Transfection, Electroporation, Reverse Transcription Polymerase Chain Reaction

Journal: Frontiers in Oncology

Article Title: YTHDF1 Aggravates the Progression of Cervical Cancer Through m 6 A-Mediated Up-Regulation of RANBP2

doi: 10.3389/fonc.2021.650383

Figure Lengend Snippet: RANBP2 is the key target of YTHDF1 in cervical cancer. (A) Western blot detecting the protein level of RANBP2 in Hela and Siha cells upon YTHDF1 knockdown. (B) RT-qPCR detecting relative RNA level of RANBP2 in Hela and Siha upon YTHDF1 knockdown. (C) RIP-PCR assays detecting the interactions between YTHDF1 and RANBP2 mRNA in Siha cells. IgG was used as an internal control. GAPDH was used as the negative control in western blot assays. (D) meRIP-PCR assays detecting the m 6 A modification of RANBP2 mRNA in Siha cells. (E) Schematic of wild-type (YTHDF1-wt) and mutant (YTHDF1-mut) YTHDF1 constructs. (F) RIP-derived RNA and protein of wild-type (YTHDF1-wt) group and mutant (YTHDF1-mut) group in Hela cells were measured by RT-qPCR and western blot after immunoprecipitation by using the antibody specific to Flag, respectively. GAPDH was used as the negative control in western blot assays. Data are shown as means ± S.D. **P < 0.01, ***P < 0.001.

Article Snippet: The slices were washed three times with PBS, and blocked with goat serum (ZSGB-BIO, ZLI-9021) at 37°C for 30 min. Rabbit anti-YTHDF1 antibody (ProteinTech, 1:100) or anti-RANBP2 antibody (ProteinTech, 1:100) was added to the slices and incubated overnight at 4°C.

Techniques: Western Blot, Knockdown, Quantitative RT-PCR, Control, Negative Control, Modification, Mutagenesis, Construct, Derivative Assay, Immunoprecipitation

Journal: Frontiers in Oncology

Article Title: YTHDF1 Aggravates the Progression of Cervical Cancer Through m 6 A-Mediated Up-Regulation of RANBP2

doi: 10.3389/fonc.2021.650383

Figure Lengend Snippet: RANBP2 plays an oncogenic role in cervical cancer cells. (A) Detection of RANBP2 knockdown in Hela and Siha cell lines by western blot. (B) The effect of RANBP2 knockdown on cell growth was determined by CCK-8 assays. (C) Colony formation assays were performed in RANBP2 knockdown and control cells. (D, E) Migration and invasion assays of Hela and Siha cells upon RANBP2 knockdown. Scale bar, 200 μm. Data are shown as means ± S.D. **P < 0.01, ***P < 0.001.

Article Snippet: The slices were washed three times with PBS, and blocked with goat serum (ZSGB-BIO, ZLI-9021) at 37°C for 30 min. Rabbit anti-YTHDF1 antibody (ProteinTech, 1:100) or anti-RANBP2 antibody (ProteinTech, 1:100) was added to the slices and incubated overnight at 4°C.

Techniques: Knockdown, Western Blot, CCK-8 Assay, Control, Migration

Journal: Frontiers in Oncology

Article Title: YTHDF1 Aggravates the Progression of Cervical Cancer Through m 6 A-Mediated Up-Regulation of RANBP2

doi: 10.3389/fonc.2021.650383

Figure Lengend Snippet: Knockdown of RANBP2 suppressed the proliferation, migration and invasion of YTHDF1-overexpressing Hela and Siha cells. (A) Colony formation assays were performed in YTHDF1-overexpressing Hela and Siha cells infected with the RANBP2 shRNA or controls. (B) The proliferation ability of YTHDF1-overexpressing Hela and Siha cells upon RANBP2 knockdown was assessed by CCK-8 assays. (C, D) Migration and invasion YTHDF1-overexpressing Hela (C) and Siha (D) cells upon RANBP2 knockdown was detected by transwell assays. Scale bar, 200 μm. *P < 0.05,**P < 0.01, ***P < 0.001.

Article Snippet: The slices were washed three times with PBS, and blocked with goat serum (ZSGB-BIO, ZLI-9021) at 37°C for 30 min. Rabbit anti-YTHDF1 antibody (ProteinTech, 1:100) or anti-RANBP2 antibody (ProteinTech, 1:100) was added to the slices and incubated overnight at 4°C.

Techniques: Knockdown, Migration, Infection, shRNA, CCK-8 Assay

Journal: Frontiers in Oncology

Article Title: YTHDF1 Aggravates the Progression of Cervical Cancer Through m 6 A-Mediated Up-Regulation of RANBP2

doi: 10.3389/fonc.2021.650383

Figure Lengend Snippet: The expression of RANBP2 is positively correlated with YTHDF1 in cervical cancer. (A) Representative immunohistochemical images of RANBP2 protein expression in cervical cancer tissues and cervical epithelium tissues. Scale bar, 100 μm. (B) The quantitative analysis of RANBP2 expression in cervical cancer tissues and cervical epithelium tissues assessed by immunohistochemistry. (C) Spearman’s correlation analysis of RANBP2 and YTHDF1 expression in cervical cancer tissues. (D) Representative immunohistochemical images of YTHDF1 and RANBP2 in the cervical cancer tissues. Scale bar, 100 μm. Data are shown as means ± S.D. *P < 0.05.

Article Snippet: The slices were washed three times with PBS, and blocked with goat serum (ZSGB-BIO, ZLI-9021) at 37°C for 30 min. Rabbit anti-YTHDF1 antibody (ProteinTech, 1:100) or anti-RANBP2 antibody (ProteinTech, 1:100) was added to the slices and incubated overnight at 4°C.

Techniques: Expressing, Immunohistochemical staining, Immunohistochemistry