anti lamc2  (Proteintech)

Journal: Frontiers in Physiology

Article Title: Molecular mechanism of Danshen injection in treating endometrial fibrosis induced by intrauterine adhesions via the LAMC2-CD44-TGF-β1-SMAD2/3 signaling pathway

doi: 10.3389/fphys.2026.1794215

Figure Lengend Snippet: LPS induced activation of rat uterine fibroblasts. (A) WB detection of LAMC2 expression levels in epithelial cells, (B) Relative expression of LAMC2 in epithelial cells, (C) Level of LAMC2 in cells detected by ELISA in epithelial cells, (D) WB detection of E-cad, N-cad, α-SMA,TGF-β1, SMAD2/3 in fibroblasts, (E) Relative expression of E-cad, N-cad, α-SMA,TGF-β1, SMAD2, SMAD3 in fibroblasts, (F) Immunofluorescence staining of COL1A1 in fibroblasts, (G) Immunofluorescence staining of COL3A1 in fibroblasts, (H) Immunofluorescence staining of α-SMA in fibroblasts, (I) Mean fluorescence intensity of COL1A1, COL3A1 and α-SMA. Compared to model in fibroblasts, * P < 0.05, ** P < 0.01.

Article Snippet: Primary antibodies: CK-19 (1:1000; YM8269, Immunoway, USA), Vimentin (1:1000; YM8324, Immunoway, USA), GAPDH (1:1000; A19056, ABclonal, China), LAMC2 (1:1000; A1869, ABclonal, China), E-cad (1:1000; A20798, ABclonal, China), N-cad (1:500; A0433, ABclonal, China), α-SMA (1:1000; A2319, ABclonal, China), TGF-β1 (1:2000; A15103, ABclonal, China), SMAD2 (1:5000; bsm-52223R, Bioss, China), SMAD3 (1:1000; A16913, ABclonal, China), p- SMAD2 (1:5000; bs-3419R, Bioss, China), p- SMAD3 (1:2000; Ap0727, ABclonal, China), and a secondary antibody (1:2000; AS014, ABclonal, China).

Techniques: Activation Assay, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Fluorescence

Journal: Frontiers in Physiology

Article Title: Molecular mechanism of Danshen injection in treating endometrial fibrosis induced by intrauterine adhesions via the LAMC2-CD44-TGF-β1-SMAD2/3 signaling pathway

doi: 10.3389/fphys.2026.1794215

Figure Lengend Snippet: Danshen injection improves endometrial fibrosis in IUA rats by inhibiting the LAMC2-CD44-TGF-β1- SMAD2/3 signaling pathway. (A) Uterine Weight, (B) Uterine Length, (C) Grading of intrauterine adhesions in each group, (D) Number of uterine glands, (E) Collagen volume fraction, (F) H&E Staining, (G) MASSON Staining, (H) Immunofluorescence staining of COL1A1, (I) Immunofluorescence staining of COL3A1, (J) Immunofluorescence staining of α-SMA, (K) Mean fluorescence intensity of COL1A1, COL3A1 and α-SMA, L: WB detection of LAMC2, TGF-β1, SMAD2, SMAD3, (L) Relative expression of protein LAMC2, TGF-β1, SMAD2, SMAD3. Compared to model, * P < 0.05, ** P < 0.01. For panels A-C, n = 6 independent animals per group; for panels (D–M) , n=3 independent animals per group.

Article Snippet: Primary antibodies: CK-19 (1:1000; YM8269, Immunoway, USA), Vimentin (1:1000; YM8324, Immunoway, USA), GAPDH (1:1000; A19056, ABclonal, China), LAMC2 (1:1000; A1869, ABclonal, China), E-cad (1:1000; A20798, ABclonal, China), N-cad (1:500; A0433, ABclonal, China), α-SMA (1:1000; A2319, ABclonal, China), TGF-β1 (1:2000; A15103, ABclonal, China), SMAD2 (1:5000; bsm-52223R, Bioss, China), SMAD3 (1:1000; A16913, ABclonal, China), p- SMAD2 (1:5000; bs-3419R, Bioss, China), p- SMAD3 (1:2000; Ap0727, ABclonal, China), and a secondary antibody (1:2000; AS014, ABclonal, China).

Techniques: Injection, Staining, Immunofluorescence, Fluorescence, Expressing

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Airway remodeling and LAMC2 upregulation are observed in both COPD patients and mouse models. ( A ) Representative Masson’s trichrome-stained lung sections from non-smokers (n=5), smokers without COPD (n=5), and COPD patients (n=5). Scale bar: 250μm. ( B ) Quantitative staining of Masson content in non-smoker (n=5), smoker (n=5), and COPD (n=5). ( C ) Representative Masson’s trichrome staining of lung sections from air-exposed control mice (n=5) and COPD model mice (n=5). Scale bar: 100μm. ( D ) Quantitative staining of Masson content in air-control (n=5) and COPD model mice (n=5). ( E ) LAMC2 expression levels in airway epithelial cells from non-smokers (n=12), smokers (n=12), and COPD patients (n=6) based on the GSE5058 dataset. ( F ) Representative airway LAMC2 immunohistochemical staining on lung sections of non-smoker (n=5), smoker (n=5), and COPD (n=5). Scale bar: 50μm. ( G ) Quantitative staining of LAMC2 intensity on airway epithelium of non-smoker (n=5), smoker (n=5), and COPD (n=5). ( H ) LAMC2 expression levels in lung tissues from air-control (n=30) and COPD model mice (n=34) based on the GSE87292 dataset. ( I ) Western blot and ( J ) quantitative analysis of LAMC2 protein expression in the lung tissue from mice from different groups (n=3 mice/group). ( K ) Representative airway LAMC2 immunohistochemical staining on lung sections of air-control (n=5) and COPD model mice (n=5).Scale bar: 100μm. ( L ) Quantitative staining of LAMC2 intensity on airway epithelium of air-control (n=5) and COPD model mice (n=5). Data presented as the means ± SD. * P < 0.05, ** P < 0.01.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Staining, Control, Expressing, Immunohistochemical staining, Western Blot

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Knockdown of LAMC2 attenuates airway remodeling and EMT in a COPD model. ( A ) Schematic overview of the animal experimental design and grouping. ( B ) Representative Masson staining on mice lung sections from different groups (n = 5 per group). ( C ) Quantitative staining of Masson content in different groups (n = 5 per group). ( D ) Representative airway Fibronectin immunohistochemical staining and ( E ) quantitative staining of Fibronectin intensity on lung sections of different groups (n = 5 per group). ( F ) Representative airway N-cadherin immunohistochemical staining and ( G ) quantitative staining of N-cadherin intensity on lung sections of different groups (n=5 per group). ( H ) Representative airway E-cadherin immunohistochemical staining and ( I ) quantitative staining of E-cadherin intensity on lung sections of different groups (n=5 per group). ( J – M ) Western blot analysis and quantification of EMT-related proteins (Fibronectin, N-cadherin, and E-cadherin) in lung tissues from the different treatment groups. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bars: 100μm.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Knockdown, Staining, Immunohistochemical staining, Western Blot

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: LAMC2 expression is upregulated in bronchial epithelial cells following TGF-β1 stimulation. ( A and B ) Volcano plots illustrating DEGs from ( A ) GSE104908 and ( B ) GSE40374 datasets, with corresponding LAMC2 expression levels. Significantly upregulated genes (red) and downregulated genes (blue) are indicated (fold change >1.5, adjusted P < 0.05). ( C ) The mRNA levels of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. ( D ) Western blot and ( E – H ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Expressing, Western Blot

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Knockdown of LAMC2 reverses TGF-β1-induced EMT marker expression and inhibits 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with different siLAMC2 constructs. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after siLAMC2 transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after siLAMC2 transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Knockdown, Marker, Expressing, Migration, Transfection, Construct, Western Blot, Wound Healing Assay

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Overexpression of LAMC2 promotes TGF-β1-induced EMT and enhances 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with LAMC2 plasmid and TGF-β1treatment. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after LAMC2 plasmid vector transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after LAMC2 plasmid vector transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Over Expression, Migration, Expressing, Transfection, Plasmid Preparation, Western Blot, Wound Healing Assay

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: LAMC2 facilitates EMT in 16HBE cells through activation of the AKT signaling pathway. ( A ) GO enrichment analysis of down-regulated DEGs from RNA-seq data, showing the top three most significantly enriched terms in each category: Biological Process (BP), Cellular Component (CC), and Molecular Function (MF) (adjusted P < 0.05). Terms are ranked by gene count. ( B ) KEGG pathway analysis of down-regulated DEGs. Statistically significant pathways (adjusted P < 0.05) are visualized in a dot plot. ( C ) Western Blot and ( D ) Immunofluorescence detection, and ( E – G ) the relative protein level of AKT and p-AKT after si-NC/LAMC2 transfection and TGF-β1 treatment. ( H ) Western Blot and ( I ) Immunofluorescence detection, and ( J – L ) the relative protein level of AKT and p-AKT after LAMC2 plasmid vector transfection and TGF-β1 treatment. Scale bar: 50 μm. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Activation Assay, RNA Sequencing, Western Blot, Immunofluorescence, Transfection, Plasmid Preparation

Journal: bioRxiv

Article Title: Cell-of-Origin, not Oncogenic Effect, Determines Desmoplastic Immune Exclusion in KRAS-Driven Liver Cancer

doi: 10.64898/2026.03.24.711280

Figure Lengend Snippet: Multi-omics integration identifies LAMC2, uPA and BSSP-4 as CCA-specific secreted factors. (A) Schematic of the experimental workflow to collect material for secretome and proteome analysis. (B) Venn diagram showing the overlap of PK-induced transcriptional and secretory responses in chol-orgs. Intersections include PK-upregulated genes in chol-orgs from RNA-seq (chol-PK vs chol-WT, bottom-left), PK-upregulated proteins in chol-orgs from secretome (CCM, bottom-right), genes whose PK-induced expression is stronger in interaction effects (interaction contrast, upper-right), and proteins predicted to be secreted according to the Human Protein Atlas (upper-left). (C) Bubble plot showing cross-dataset support for candidate PK-associated genes identified by the integrative analysis in (B). Rows indicate 15 selected genes from (B), and columns indicate the indicated in-house murine result and public human datasets. Dot color encodes z-scored log2 FC (z(LFC). Filled circles indicate significant differences (padj < 0.1) and open circles indicate non-significant results. Dot size reflects statistical strength-log10(padj).

Article Snippet: The antibodies used in this study were: Lamc2 (Proteintech, #19698-1-AP), uPA (Proteintech, #17968-1-AP), BSSP4 (ThermoFisher Scientific, #PA5-47245), and rabbit-IgG (Millipore, #pp64).

Techniques: Biomarker Discovery, RNA Sequencing, Expressing

Journal: bioRxiv

Article Title: Cell-of-Origin, not Oncogenic Effect, Determines Desmoplastic Immune Exclusion in KRAS-Driven Liver Cancer

doi: 10.64898/2026.03.24.711280

Figure Lengend Snippet: LAMC2 and uPA affect HSC activation and impair CCA formation in vivo . (A) Schematic overview of the in vitro fibroblast activation assay, where murine HSCs were treated with CCM from chol-PK and neutralizing antibodies. (B) Scatter plot indicating mRNA expression of Acta2 and Col1a1 in mHSCs treated with Chol-PK CCM and indicated neutralizing antibodies or control IgG. (n=5 from 2 independent experiments). (C) Schematic of scratch assay with mHSCs treated with low FBS (2%) media supplemented with respective recombinant protein. (D) Plot depicting mean relative wound coverage upon scratch injury over time with indicated recombinant protein at different dosage (n≥17 from 3 experiments). (E) Schematic of in vivo validation model: Chol-PK organoids were edited by CRISPR/Cas9 to generate Prss22 -, Lamc2 -, or Plau -deleted lines, which were orthotopically implanted into the liver and harvested at the same time point. (F) Macroscopic images of liver tumors 7 weeks after implantation of indicated lines. (G) Bar plot with respective tumor penetrance per line. (H) Representative histopathology images of liver tumors obtained upon orthotopic implantation of chol-PK and indicated KO lines. Stains as indicated. Red dotted line demarcates the boundary between non-tumor liver (N) and tumor (T). All scale bars are 100 μm. (I) Scatter plot depicting the total CD3 + and CD8 + T cell density per area per tumor for the indicated lines.

Article Snippet: The antibodies used in this study were: Lamc2 (Proteintech, #19698-1-AP), uPA (Proteintech, #17968-1-AP), BSSP4 (ThermoFisher Scientific, #PA5-47245), and rabbit-IgG (Millipore, #pp64).

Techniques: Activation Assay, In Vivo, In Vitro, Expressing, Control, Wound Healing Assay, Recombinant, Biomarker Discovery, CRISPR, Histopathology