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ATCC mouse chl1

Figure 3. <t>Chl1</t> is a direct target of miR-10a-5p (A) The public miRNA databases (TargetScan) predict that Chl1 may be a target for miR-10a-5p and that the 3′-UTR of Chl1 mRNA contains a highly conserved and complementary sequence between positions 2815 and 2821 for the binding of the seed sequence of miR-10a-5p. (B) Cells were transfected with pMIR-Chl1-WT, pMIR-Chl1-MUT or miR-10a-5p positive control (PC) reporter plasmids together with miR-10a-5p mimics or negative controls. The levels of firefly and Renilla luciferase activities were assayed 24 and 48 h later. (C) Relative expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NTD tissues and normal tissues (NCs) at E8.5, E9.5 and E10.5. (D) The expression of the Chl1 protein in NTD and NC tissues at E9.5 and E10.5 was measured by western blot analysis. (E) Representative micrographs of immunofluorescence staining for Chl1 (red) with nuclei stained blue with DAPI. Areas of Chl1-positive cells were quantified by using ImageJ. (F) The expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NSCs after transfection with LV-miR-10a or LV-NC for 48 h (left). Relative Chl1 protein expression in NSCs after transfection with LV-miR-10a or LV-NC for 72 h was measured by western blot analysis using GAPDH as an internal control (right). Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Mouse Chl1, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 125 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1 ."

Article Title: Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1 .

Journal: Acta biochimica et biophysica Sinica

doi: 10.3724/abbs.2024078

Figure 3. Chl1 is a direct target of miR-10a-5p (A) The public miRNA databases (TargetScan) predict that Chl1 may be a target for miR-10a-5p and that the 3′-UTR of Chl1 mRNA contains a highly conserved and complementary sequence between positions 2815 and 2821 for the binding of the seed sequence of miR-10a-5p. (B) Cells were transfected with pMIR-Chl1-WT, pMIR-Chl1-MUT or miR-10a-5p positive control (PC) reporter plasmids together with miR-10a-5p mimics or negative controls. The levels of firefly and Renilla luciferase activities were assayed 24 and 48 h later. (C) Relative expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NTD tissues and normal tissues (NCs) at E8.5, E9.5 and E10.5. (D) The expression of the Chl1 protein in NTD and NC tissues at E9.5 and E10.5 was measured by western blot analysis. (E) Representative micrographs of immunofluorescence staining for Chl1 (red) with nuclei stained blue with DAPI. Areas of Chl1-positive cells were quantified by using ImageJ. (F) The expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NSCs after transfection with LV-miR-10a or LV-NC for 48 h (left). Relative Chl1 protein expression in NSCs after transfection with LV-miR-10a or LV-NC for 72 h was measured by western blot analysis using GAPDH as an internal control (right). Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Figure Legend Snippet: Figure 3. Chl1 is a direct target of miR-10a-5p (A) The public miRNA databases (TargetScan) predict that Chl1 may be a target for miR-10a-5p and that the 3′-UTR of Chl1 mRNA contains a highly conserved and complementary sequence between positions 2815 and 2821 for the binding of the seed sequence of miR-10a-5p. (B) Cells were transfected with pMIR-Chl1-WT, pMIR-Chl1-MUT or miR-10a-5p positive control (PC) reporter plasmids together with miR-10a-5p mimics or negative controls. The levels of firefly and Renilla luciferase activities were assayed 24 and 48 h later. (C) Relative expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NTD tissues and normal tissues (NCs) at E8.5, E9.5 and E10.5. (D) The expression of the Chl1 protein in NTD and NC tissues at E9.5 and E10.5 was measured by western blot analysis. (E) Representative micrographs of immunofluorescence staining for Chl1 (red) with nuclei stained blue with DAPI. Areas of Chl1-positive cells were quantified by using ImageJ. (F) The expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NSCs after transfection with LV-miR-10a or LV-NC for 48 h (left). Relative Chl1 protein expression in NSCs after transfection with LV-miR-10a or LV-NC for 72 h was measured by western blot analysis using GAPDH as an internal control (right). Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Techniques Used: Sequencing, Binding Assay, Transfection, Positive Control, Luciferase, Expressing, Quantitative RT-PCR, Control, Western Blot, Immunofluorescence, Staining

Figure 4. Effects of Chl1 knockdown on cell proliferation and differentiation (A) The expressions of Chl1 mRNA and protein in NSCs were measured by RT-qPCR (left) and western blot (right) analysis after transfection with siR-NC, siR1-Chl1, siR2-Chl1 or siR3-Chl1 for 72 h. (B) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly lower in the siR1-Chl1 group than in the blank or siR-NC groups. (C) FCM results of the cell cycle analysis are shown. The percentage of cells in the G1 phase was significantly greater and the percentage of cells in the S and G2 phases was significantly lower in the siR1-Chl1 group than in the blank or siR-NC groups. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly lower in the siR1-CHL1 group than in the blank or siR-NC groups. Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Figure Legend Snippet: Figure 4. Effects of Chl1 knockdown on cell proliferation and differentiation (A) The expressions of Chl1 mRNA and protein in NSCs were measured by RT-qPCR (left) and western blot (right) analysis after transfection with siR-NC, siR1-Chl1, siR2-Chl1 or siR3-Chl1 for 72 h. (B) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly lower in the siR1-Chl1 group than in the blank or siR-NC groups. (C) FCM results of the cell cycle analysis are shown. The percentage of cells in the G1 phase was significantly greater and the percentage of cells in the S and G2 phases was significantly lower in the siR1-Chl1 group than in the blank or siR-NC groups. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly lower in the siR1-CHL1 group than in the blank or siR-NC groups. Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Techniques Used: Knockdown, Quantitative RT-PCR, Western Blot, Transfection, Immunofluorescence, Staining, Cell Cycle Assay

Figure 5. Re-expression of Chl1 reverses the effect of miR-10a-5p on proliferation and differentiation of NSCs (A) Representative micrographs of GFP expression in NSCs after transfection with AV-NC or AV-Chl1 for 72 h. (B) The expression of Chl1 protein in NSCs after transfection (AV-NC or AV-Chl1) or cotransfection (LV-miR-10a or LV-NC) for 72 h was measured by western blot analysis. (C) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly greater in the LV-miR-10a+AV-Chl1 group than in the LV-miR-10a+AV-NC group. The miR-10a-5p-induced proliferation of NSCs was restored via Chl1 re-expression. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly greater in the LV-miR-10a+AV-Chl1 group than in the LV-miR-10a+AV-NC group. The miR- 10a-5p-induced differentiation of NSCs was restored by Chl1 re-expression. Scale bar: 50 μm. *P<0.05, **P<0.01; ***P<0.001.

Figure Legend Snippet: Figure 5. Re-expression of Chl1 reverses the effect of miR-10a-5p on proliferation and differentiation of NSCs (A) Representative micrographs of GFP expression in NSCs after transfection with AV-NC or AV-Chl1 for 72 h. (B) The expression of Chl1 protein in NSCs after transfection (AV-NC or AV-Chl1) or cotransfection (LV-miR-10a or LV-NC) for 72 h was measured by western blot analysis. (C) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly greater in the LV-miR-10a+AV-Chl1 group than in the LV-miR-10a+AV-NC group. The miR-10a-5p-induced proliferation of NSCs was restored via Chl1 re-expression. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly greater in the LV-miR-10a+AV-Chl1 group than in the LV-miR-10a+AV-NC group. The miR- 10a-5p-induced differentiation of NSCs was restored by Chl1 re-expression. Scale bar: 50 μm. *P<0.05, **P<0.01; ***P<0.001.

Techniques Used: Expressing, Transfection, Cotransfection, Western Blot, Immunofluorescence, Staining

Figure 6. The ERK agonist Honokiol reverses the effects of miR-10a-5p on proliferation and differentiation of NSCs (A) The protein expression levels of p-SRC, SRC, p-PI3K, PI3K, p-ERK and ERK were determined by western blot analysis in NSCs after transfection with siR-NC or siR1-Chl1 for 72 h. (B) The expression levels of p-ERK and ERK proteins were measured by western blot analysis in NSCs after treatment with DMSO or Honokiol and cotransfection with LV-miR-10a or LV-NC for 72 h. (C) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly greater in the LV-miR-10a+Honokiol group than in the LV-miR-10a+DMSO group. The miR-10a-5p-induced proliferation of NSCs was restored by Honokiol. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly greater in the LV- miR-10a+Honokiol group than in the LV-miR-10a+DMSO group. The miR-10a-5p-induced differentiation of NSCs was reversed by Honokiol. Scale bar: 50 μm. **P<0.01; ***P<0.001.

Figure Legend Snippet: Figure 6. The ERK agonist Honokiol reverses the effects of miR-10a-5p on proliferation and differentiation of NSCs (A) The protein expression levels of p-SRC, SRC, p-PI3K, PI3K, p-ERK and ERK were determined by western blot analysis in NSCs after transfection with siR-NC or siR1-Chl1 for 72 h. (B) The expression levels of p-ERK and ERK proteins were measured by western blot analysis in NSCs after treatment with DMSO or Honokiol and cotransfection with LV-miR-10a or LV-NC for 72 h. (C) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly greater in the LV-miR-10a+Honokiol group than in the LV-miR-10a+DMSO group. The miR-10a-5p-induced proliferation of NSCs was restored by Honokiol. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly greater in the LV- miR-10a+Honokiol group than in the LV-miR-10a+DMSO group. The miR-10a-5p-induced differentiation of NSCs was reversed by Honokiol. Scale bar: 50 μm. **P<0.01; ***P<0.001.

Techniques Used: Expressing, Western Blot, Transfection, Cotransfection, Immunofluorescence, Staining

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Article Title: Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1
Article Snippet: .. The human embryonic kidney cell line 293T (HEK293T; ATCC, Manassas, USA) was cultured in Dulbecco’s modified Eagle’s medium (DMEM; Sigma) supplemented with 10% fetal bovine serum and 1% Pen/Strep. mmu-miR-10a-5p and mouse Chl1 were cloned and inserted into the LVX-hEF1a-EGFP-gene-PGK-PURO and pAD-mCMV-GFP-MCS-3FLAG vectors, respectively. .. The constructs were sent to Sunbio Medical Biotechnology (Shanghai, China) for lentivirus and adenovirus packaging and purification.

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Journal: Acta biochimica et biophysica Sinica

Article Title: Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1 .

doi: 10.3724/abbs.2024078

Figure Lengend Snippet: Figure 3. Chl1 is a direct target of miR-10a-5p (A) The public miRNA databases (TargetScan) predict that Chl1 may be a target for miR-10a-5p and that the 3′-UTR of Chl1 mRNA contains a highly conserved and complementary sequence between positions 2815 and 2821 for the binding of the seed sequence of miR-10a-5p. (B) Cells were transfected with pMIR-Chl1-WT, pMIR-Chl1-MUT or miR-10a-5p positive control (PC) reporter plasmids together with miR-10a-5p mimics or negative controls. The levels of firefly and Renilla luciferase activities were assayed 24 and 48 h later. (C) Relative expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NTD tissues and normal tissues (NCs) at E8.5, E9.5 and E10.5. (D) The expression of the Chl1 protein in NTD and NC tissues at E9.5 and E10.5 was measured by western blot analysis. (E) Representative micrographs of immunofluorescence staining for Chl1 (red) with nuclei stained blue with DAPI. Areas of Chl1-positive cells were quantified by using ImageJ. (F) The expression of Chl1 mRNA was measured by RT-qPCR using β-actin as an internal control in NSCs after transfection with LV-miR-10a or LV-NC for 48 h (left). Relative Chl1 protein expression in NSCs after transfection with LV-miR-10a or LV-NC for 72 h was measured by western blot analysis using GAPDH as an internal control (right). Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Article Snippet: The human embryonic kidney cell line 293T (HEK293T; ATCC, Manassas, USA) was cultured in Dulbecco’s modified Eagle’s medium (DMEM; Sigma) supplemented with 10% fetal bovine serum and 1% Pen/Strep. mmu-miR-10a-5p and mouse Chl1 were cloned and inserted into the LVX-hEF1a-EGFP-gene-PGK-PURO and pAD-mCMV-GFP-MCS3FLAG vectors, respectively.

Techniques: Sequencing, Binding Assay, Transfection, Positive Control, Luciferase, Expressing, Quantitative RT-PCR, Control, Western Blot, Immunofluorescence, Staining

Journal: Acta biochimica et biophysica Sinica

Article Title: Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1 .

doi: 10.3724/abbs.2024078

Figure Lengend Snippet: Figure 4. Effects of Chl1 knockdown on cell proliferation and differentiation (A) The expressions of Chl1 mRNA and protein in NSCs were measured by RT-qPCR (left) and western blot (right) analysis after transfection with siR-NC, siR1-Chl1, siR2-Chl1 or siR3-Chl1 for 72 h. (B) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly lower in the siR1-Chl1 group than in the blank or siR-NC groups. (C) FCM results of the cell cycle analysis are shown. The percentage of cells in the G1 phase was significantly greater and the percentage of cells in the S and G2 phases was significantly lower in the siR1-Chl1 group than in the blank or siR-NC groups. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly lower in the siR1-CHL1 group than in the blank or siR-NC groups. Scale bar: 50 μm. *P<0.05; **P<0.01; ***P<0.001.

Techniques: Knockdown, Quantitative RT-PCR, Western Blot, Transfection, Immunofluorescence, Staining, Cell Cycle Assay

Journal: Acta biochimica et biophysica Sinica

Article Title: Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1 .

doi: 10.3724/abbs.2024078

Figure Lengend Snippet: Figure 5. Re-expression of Chl1 reverses the effect of miR-10a-5p on proliferation and differentiation of NSCs (A) Representative micrographs of GFP expression in NSCs after transfection with AV-NC or AV-Chl1 for 72 h. (B) The expression of Chl1 protein in NSCs after transfection (AV-NC or AV-Chl1) or cotransfection (LV-miR-10a or LV-NC) for 72 h was measured by western blot analysis. (C) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly greater in the LV-miR-10a+AV-Chl1 group than in the LV-miR-10a+AV-NC group. The miR-10a-5p-induced proliferation of NSCs was restored via Chl1 re-expression. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly greater in the LV-miR-10a+AV-Chl1 group than in the LV-miR-10a+AV-NC group. The miR- 10a-5p-induced differentiation of NSCs was restored by Chl1 re-expression. Scale bar: 50 μm. *P<0.05, **P<0.01; ***P<0.001.

Techniques: Expressing, Transfection, Cotransfection, Western Blot, Immunofluorescence, Staining

Journal: Acta biochimica et biophysica Sinica

Article Title: Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1 .

doi: 10.3724/abbs.2024078

Figure Lengend Snippet: Figure 6. The ERK agonist Honokiol reverses the effects of miR-10a-5p on proliferation and differentiation of NSCs (A) The protein expression levels of p-SRC, SRC, p-PI3K, PI3K, p-ERK and ERK were determined by western blot analysis in NSCs after transfection with siR-NC or siR1-Chl1 for 72 h. (B) The expression levels of p-ERK and ERK proteins were measured by western blot analysis in NSCs after treatment with DMSO or Honokiol and cotransfection with LV-miR-10a or LV-NC for 72 h. (C) Representative micrographs of immunofluorescence staining for BrdU (red) with nuclei stained blue with DAPI. Arrows indicate BrdU+ cells. The percentage of BrdU+ cells was significantly greater in the LV-miR-10a+Honokiol group than in the LV-miR-10a+DMSO group. The miR-10a-5p-induced proliferation of NSCs was restored by Honokiol. (D) Representative micrographs of immunofluorescence staining for GFAP (red) with nuclei stained blue with DAPI. The percentage of GFAP+ cells was significantly greater in the LV- miR-10a+Honokiol group than in the LV-miR-10a+DMSO group. The miR-10a-5p-induced differentiation of NSCs was reversed by Honokiol. Scale bar: 50 μm. **P<0.01; ***P<0.001.

Techniques: Expressing, Western Blot, Transfection, Cotransfection, Immunofluorescence, Staining

Fig. 5 Quantitative proteomics in Rab35 cKO P0 hippocampus. a Volcano plot of the TMT-based quantitative proteomes identifying the dysregulated proteins in Rab35 cKO hippocampus in comparison with the control hippocampus (n = 5 mice per genotype). b Number of proteins identiﬁed as signiﬁcantly dysregulated and as either membrane trafﬁc-related or neuronal migration-related. c, d Western blot analysis of control and Rab35 cKO P0 hippocampi using anti-contactin-2, anti-CHL1, and anti-actin antibodies. e, f Quantiﬁcation of contactin-2 (c) and CHL1 (d) protein levels in control and Rab35 cKO P0 hippocampi. Band intensities of the indicated proteins were normalized to those of actin (n = 9 mice per genotype). Unpaired Student’s t- test; e, p = 0.0153; f, p = 0.0095. g, h Levels of contactin-2 (g) and CHL1 (h) were quantiﬁed by targeted MS using the PRM method (n = 5 mice per genotype). Unpaired Student’s t-test; g p = 0.0053; h p = 0.0229. i Western blot analysis of control and Rab35 cKO P0 hippocampus using anti-N-cadherin and anti-actin antibodies. j Quantiﬁcation of N-cadherin protein levels in the control and Rab35 cKO P0 hippocampus (n = 9 mice per genotypes). Unpaired Student’s t-test, p = 0.9020. k Representative images of DIV 2 hippocampal primary neurons stained for contactin-2 (green), rhodamine-phalloidin (magenta) and DAPI (blue). Scale bar, 20 μm. l Quantiﬁcation of contactin-2 intensity at the somatic plasma membrane in control (n = 4) and Rab35- deﬁcient (n = 4) cells. Thirty neurons from four different cultures per genotype were analyzed. Mann–Whitney U-test, p = 0.0286. Data represent the mean ± SEM; n.s. not signiﬁcant (p > 0.05); *p < 0.05; **p < 0.01.

Journal: Communications biology

Article Title: RAB35 is required for murine hippocampal development and functions by regulating neuronal cell distribution.

doi: 10.1038/s42003-023-04826-x

Figure Lengend Snippet: Fig. 5 Quantitative proteomics in Rab35 cKO P0 hippocampus. a Volcano plot of the TMT-based quantitative proteomes identifying the dysregulated proteins in Rab35 cKO hippocampus in comparison with the control hippocampus (n = 5 mice per genotype). b Number of proteins identiﬁed as signiﬁcantly dysregulated and as either membrane trafﬁc-related or neuronal migration-related. c, d Western blot analysis of control and Rab35 cKO P0 hippocampi using anti-contactin-2, anti-CHL1, and anti-actin antibodies. e, f Quantiﬁcation of contactin-2 (c) and CHL1 (d) protein levels in control and Rab35 cKO P0 hippocampi. Band intensities of the indicated proteins were normalized to those of actin (n = 9 mice per genotype). Unpaired Student’s t- test; e, p = 0.0153; f, p = 0.0095. g, h Levels of contactin-2 (g) and CHL1 (h) were quantiﬁed by targeted MS using the PRM method (n = 5 mice per genotype). Unpaired Student’s t-test; g p = 0.0053; h p = 0.0229. i Western blot analysis of control and Rab35 cKO P0 hippocampus using anti-N-cadherin and anti-actin antibodies. j Quantiﬁcation of N-cadherin protein levels in the control and Rab35 cKO P0 hippocampus (n = 9 mice per genotypes). Unpaired Student’s t-test, p = 0.9020. k Representative images of DIV 2 hippocampal primary neurons stained for contactin-2 (green), rhodamine-phalloidin (magenta) and DAPI (blue). Scale bar, 20 μm. l Quantiﬁcation of contactin-2 intensity at the somatic plasma membrane in control (n = 4) and Rab35- deﬁcient (n = 4) cells. Thirty neurons from four different cultures per genotype were analyzed. Mann–Whitney U-test, p = 0.0286. Data represent the mean ± SEM; n.s. not signiﬁcant (p > 0.05); *p < 0.05; **p < 0.01.

Article Snippet: The following primary antibodies were used for immunoblotting: 1:1000 RAB35 (rabbit; Cell Signaling, 9690 S), 1:10,000 Actin [C4] (mouse; MerckMillipore, MAB1501), 1:10,000 GAPDH [6C5] (mouse; Merck-Millipore, MAB374), 1:1000 contactin-2/TAG-1 (goat; R&D systems, AF4439), 1:1000 CHL1 (goat; R&D systems, AF2147), and 1:1000 N-cadherin [32/N-cadherin] (rabbit; BD, 610920).

Techniques: Quantitative Proteomics, Comparison, Control, Membrane, Migration, Western Blot, Staining, Clinical Proteomics, MANN-WHITNEY

Fig. 4 STORM imaging of transmembrane proteins or membrane-bound signaling proteins associated with the MPS. a Left: 3D STORM images of two potassium channel subunits, Kv 1.2 and Kv 1.3, in axons. Middle: 1D autocorrelation of the imaged proteins for the axon region indicated by the dashed line in the left panels. Right: Average 1D autocorrelation of the imaged proteins over 20–90 randomly chosen axon regions. b Same as (a) but for ﬁve cell adhesion molecules, including neurofascin, NrCAM, L1CAM, NCAM1 and CHL1. c Same as (a) but for three membrane-associated (non-transmembrane) signaling molecules, including calcium/calmodulin-dependent protein kinase type IIβ (CAMK IIβ), heterotrimeric G protein β-subunit 1, and brain acid soluble protein 1, as well as a transmembrane signaling molecule, glycoprotein M6A. STORM images in a–c are representative examples from three independent experiments with similar results. Scale bars: 1 μm. Source data are provided as a Source Data ﬁle.

Journal: Nature communications

Article Title: Proteomic and functional analyses of the periodic membrane skeleton in neurons.

doi: 10.1038/s41467-022-30720-x

Figure Lengend Snippet: Fig. 4 STORM imaging of transmembrane proteins or membrane-bound signaling proteins associated with the MPS. a Left: 3D STORM images of two potassium channel subunits, Kv 1.2 and Kv 1.3, in axons. Middle: 1D autocorrelation of the imaged proteins for the axon region indicated by the dashed line in the left panels. Right: Average 1D autocorrelation of the imaged proteins over 20–90 randomly chosen axon regions. b Same as (a) but for ﬁve cell adhesion molecules, including neurofascin, NrCAM, L1CAM, NCAM1 and CHL1. c Same as (a) but for three membrane-associated (non-transmembrane) signaling molecules, including calcium/calmodulin-dependent protein kinase type IIβ (CAMK IIβ), heterotrimeric G protein β-subunit 1, and brain acid soluble protein 1, as well as a transmembrane signaling molecule, glycoprotein M6A. STORM images in a–c are representative examples from three independent experiments with similar results. Scale bars: 1 μm. Source data are provided as a Source Data ﬁle.

Article Snippet: The following primary antibodies were used in this study: guinea pig anti-MAP2 antibody 1:500 dilution for immunofluorescence (IF) (Synaptic Systems, 188004), rabbit anti-MAP2 antibody 1:500 for IF (Synaptic Systems, 188002), mouse anti-αII spectrin antibody 1:400 for IF (Biolegend, 803201, Clone D8B7), mouse anti-αII spectrin antibody 1:200 for IF (Encor Biotechnology, MCA-3D7, Clone 3D7), rabbit anti-αII spectrin antibody 1:200 for IF (Encor Biotechnology, RPCA-aII-Spec), mouse anti-αII spectrin antibody 1:200 for IF (EMD Millipore, MAB1622, Clone AA6), mouse anti-βII spectrin antibody 1:200 for IF (BD Biosciences, 612563, Clone 42), mouse anti-dematin antibody 1:50 for IF (Santa Cruz Biotechnology, sc-135881, Clone 18), rabbit anti-coronin 2B antibody 1:200 for IF (Novus Biologicals, NBP 1-85567), mouse anti-tubulin antibody 1:100 for IF (Santa Cruz Biotechnology, sc-5286, Clone B7), rabbit anti-Tau antibody 1:500 for IF (Synaptic Systems, 314002), mouse anti-Kv1.2 channel antibody 1:200 for IF (Neuromab, 75-008, Clone K14/16), rabbit anti-neurofascin antibody 1:200 for IF (Neuromab, 75–172, Clone A12/18), rabbit anti-NrCAM 1:200 for IF (Abcam, ab24344), goat anti-CHL1 antibody 1:200 for IF (R&D systems, AF2147), rabbit anti-NCAM1 antibody 1:200 for IF (EMD Millipore, AB5032), mouse anti-ankyrin G antibody 1:100 for IF (Santa Cruz Biotechnology, sc-12719, Clone 463), mouse anti-bassoon antibody 1:400 for IF (Enzo, ADI-VAM-PS003-F, Clone SAP7F407), rabbit anti-homer antibody 1:500 for IF (Synaptic Systems, 160003), rabbit antiL1CAM antibody 1:500 for Western blot (WB) (ABclonal, A8555), rat antiL1CAM antibody 1:200 for IF (R&D Systems, MAB5674, Clone 555), rabbit antiNMIIB (Myh10) (N-terminus) antibody 1:200 for IF (GeneTex, GTX133378), rabbit anti-NMIIA (Myh9) (N-terminus) antibody 1:200 for IF (GeneTex, GTX101751), rabbit anti-NMIIB (Myh10) (C-terminus) antibody 1:200 for IF (Biolegend, 909901), rabbit anti-Glutamate Receptor 2 & 3 antibody 1:200 for IF (EMD Millipore, AB1506), rabbit anti-GFP antibody 1:400 for IF (Thermo Fisher Scientific, A11122). rabbit anti-β-actin antibody 1:1000 for WB (Proteintech, 20536-1-AP).

Techniques: Imaging, Membrane

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