Journal: Aging (Albany NY)

Article Title: FK506 binding protein 10: a key actor of collagen crosslinking in clear cell renal cell carcinoma

doi: 10.18632/aging.203359

Figure Lengend Snippet: FKBP10, PLOD2 and pro-collagen I shows high transcription level in ccRCC. Levels of FKBP10, PLOD2 and pro-collagen I mRNA were significantly higher in ccRCC than in normal tissue. Fold change, associated p values, and overexpression gene rank are shown. ( A ) FKBP10 mRNA expression level in Gumz Renal dataset. FKBP10 presented a fold change of 13.212, ranking top 2% in overexpression gene. ( B ) PLOD2 mRNA expression level in Gumz Renal dataset. PLOD2 presented a fold change of 4.249, ranking top 2% in overexpression gene. ( C ), ( D ) COL1A1 and COL1A2 mRNA expression level in Gumz Renal dataset. COL1A1 and COL1A2 presented a fold change of 3.850 and 9.055 respectively, both ranking top 2% in overexpression gene.

Article Snippet: Monoclonal mouse anti-FKBP10 antibody (sc-135907), monoclonal mouse anti-actin antibody (sc-8432), monoclonal mouse anti-CHOP antibody (sc-7351), monoclonal mouse anti-COL1A1 antibody (sc-293182) was purchased from Santa Cruz.

Techniques: Over Expression, Expressing

Journal: Aging (Albany NY)

Article Title: FK506 binding protein 10: a key actor of collagen crosslinking in clear cell renal cell carcinoma

doi: 10.18632/aging.203359

Figure Lengend Snippet: Genes correlated with FKBP10 and PLOD2 in ccRCC, and PPI network of FKBP10. ( A ) Heat map showing top50 genes positively correlated with FKBP10 in ccRCC, PLOD2 was ranked. ( B ) Heat map showing top50 genes positively correlated with PLOD2 in ccRCC, FKBP10 was ranked. ( C ) PPI network of FKBP10 analyzed by String database. PLOD2, COL1A1 and COL1A2 showed strong interaction with FKBP10 (interaction score > 0.7).

Article Snippet: Monoclonal mouse anti-FKBP10 antibody (sc-135907), monoclonal mouse anti-actin antibody (sc-8432), monoclonal mouse anti-CHOP antibody (sc-7351), monoclonal mouse anti-COL1A1 antibody (sc-293182) was purchased from Santa Cruz.

Techniques:

Journal: Aging (Albany NY)

Article Title: FK506 binding protein 10: a key actor of collagen crosslinking in clear cell renal cell carcinoma

doi: 10.18632/aging.203359

Figure Lengend Snippet: Gene Ontology analysis reports FKBP10 and its correlated genes are densely involved in collagen synthesis. ( A ) Molecular function analysis of FKBP10 in ccRCC: collagen binding (GO:0005518), extracellular matrix structural constituent conferring tensile strength (GO:0030020), cis-trans isomerase activity (GO:0016859). ( B ) Biological process analysis of FKBP10 in ccRCC: collagen fibril organization (GO:0030199), extracellular matrix organization (GO:0030198), peptidyl-proline modification (GO:0018208), peptidyl-lysine hydroxylation (GO:0017185), collagen metabolic process (GO:0032963). ( C ) Cellular component analysis of FKBP10 in ccRCC:: endoplasmic reticulum lumen (GO:0005788), endoplasmic reticulum (GO:0005783), collagen type I trimer (G:0005584), collagen trimer (GO:0005581), fibrillar collagen trimer (GO:0005583), banded collagen fibril (GO:0098643), complex of collagen trimers (GO:0098644).

Article Snippet: Monoclonal mouse anti-FKBP10 antibody (sc-135907), monoclonal mouse anti-actin antibody (sc-8432), monoclonal mouse anti-CHOP antibody (sc-7351), monoclonal mouse anti-COL1A1 antibody (sc-293182) was purchased from Santa Cruz.

Techniques: Binding Assay, Activity Assay, Modification

Journal: Aging (Albany NY)

Article Title: FK506 binding protein 10: a key actor of collagen crosslinking in clear cell renal cell carcinoma

doi: 10.18632/aging.203359

Figure Lengend Snippet: FKBP10 is high expressed and its inhibition causes ER stress in ccRCC. β-actin is set as loading control. Quantitative analysis of each study is presented in a bar graph. ( A ) Immunoblotting showed FKBP10 was high expressed in 786-O ccRCC cell line comparing with normal kidney HK-2 cell line. ( B ) FKBP10 RNAi efficacy was confirmed by immunoblotting. ( C ) After FKBP10 RNAi, ER stress marker CHOP was high expressed than negative control group. ( D ) After FKBP10 RNAi, collagen type I precursor COL1A1 aberrantly accumulated in ccRCC cells. Negative control group showed much less expression of COL1A1.

Article Snippet: Monoclonal mouse anti-FKBP10 antibody (sc-135907), monoclonal mouse anti-actin antibody (sc-8432), monoclonal mouse anti-CHOP antibody (sc-7351), monoclonal mouse anti-COL1A1 antibody (sc-293182) was purchased from Santa Cruz.

Techniques: Inhibition, Control, Western Blot, Marker, Negative Control, Expressing

Journal: Biological Research

Article Title: MicroRNA-98 inhibits the cell proliferation of human hypertrophic scar fibroblasts via targeting Col1A1

doi: 10.1186/s40659-017-0127-6

Figure Lengend Snippet: a Predicted miR-98 binding sites within the 3′-UTR of Col1A1mRNA. b The wt or mt reporter plasmid was cotransfected into HSBFs with miR-98 inhibitor, inhibitor NC, miR-98 mimic or mimic NC. Luciferase activity of pGL3-Col1A1 was increased significantly by miR-98 inhibitor and decreased markedly by miR-98 mimic. c Protein expression of Col1A1 after HSFB transfecting with miR-98 inhibitor, inhibitor NC, miR-98 mimic or mimic NC

Article Snippet: The mouse monoclonal anti-human Col1A1 antibody (R&D Systems Europe Ltd.) was diluted 1:500.

Techniques: Binding Assay, Plasmid Preparation, Luciferase, Activity Assay, Expressing

Journal: Biological Research

Article Title: MicroRNA-98 inhibits the cell proliferation of human hypertrophic scar fibroblasts via targeting Col1A1

doi: 10.1186/s40659-017-0127-6

Figure Lengend Snippet: Inverse correlation of miR-98 and Col1A1 expression of in HS tissues

Article Snippet: The mouse monoclonal anti-human Col1A1 antibody (R&D Systems Europe Ltd.) was diluted 1:500.

Techniques: Expressing

Journal: Molecular Systems Biology

Article Title: Synovial matrix turnover controls immune cell spatial patterning in inflammation resolution

doi: 10.1038/s44320-025-00149-7

Figure Lengend Snippet: Raw data and cells from the Alivernini dataset were analysed de novo to subset out fibroblasts as detailed in Appendix Fig. . Fibroblasts were subsequently reclustered into four fibroblast clusters using the Zhang dataset nomenclature (AMP1-like) (Zhang et al, ; Data ref: Zhang et al, ) to enable direct comparison of cell types across studies. Newly subsetted fibroblasts were also clustered using the matrisome gene list, excluding cytokines and chemokines, with their top cluster-defining markers chosen to investigate protein distribution in human RA synovial tissue via multiplexed immunofluorescence. ( A ) UMAP of the Alivernini dataset fibroblast clustered using the full available genome to redefine AMP1-like clusters (top) or using the cytokine- and chemokine-subtracted matrisome to identify matrix-defined clusters (bottom). ( B) Alluvial plot of the label-transfer and contributions of synovial fibroblasts in the AMP1-like clusters to the matrix-defined clusters. ( C ) Table of the percentage of cells from each AMP1-like cluster that make up each of the matrix-defined clusters. ( D ) Heatmap of the top ten cluster-defining matrix genes for each of the matrix-defined clusters. ( E ) Representative immunofluorescent staining on human RA patient synovial biopsies for key fibroblast cluster and niche-defining matrix markers fibronectin (FN), IGFBP5, IGFBP7, MFAP5, and type I collagen (COL1A1). FN, MFAP5 and COL1A1 stains were performed on biopsies from N = 3 donors; IGFBP5 and IGFBP7 on biopsies from N = 6 donors. .

Article Snippet: Rabbit anti-human COL1A1 , Cell Signalling Technologies , 28368S.

Techniques: Comparison, Immunofluorescence, Staining

Journal: Molecular Systems Biology

Article Title: Synovial matrix turnover controls immune cell spatial patterning in inflammation resolution

doi: 10.1038/s44320-025-00149-7

Figure Lengend Snippet: Following differential expression analysis between newly defined AMP1-like fibroblast clusters of the Alivernini dataset, DEGs were prioritised based on DEG conservation between differential expression analysis methods edgeR and MAST, conservation in a newly performed MAST analysis of the Wei mouse dataset of STIA, log2FC and adjusted P values. ( A ) Ranks of the top ten prioritised matrisomal DEGs in active RA/remission lining and sub-lining fibroblasts. ( B ) Network analysis of protein abundances and correlations in Graphia. Each protein is represented by a dot. Protein clusters are grouped by colour, with orange proteins corresponding to proteins more abundant in RA, green proteins more abundant in OA, and purple and yellow proteins in neither. ( N = 12 for OA and N = 10 for RA). ( C ) Heatmaps of protein abundance for proteins found to be overrepresented in RA (orange) and OA (green) samples. Stars denote a P value < 0.05 through t test. ( N = 12 for OA and 10 for RA). ( D ) Abundance of Collagen-I and VI protein in OA and RA patient samples ( N = 12 and N = 10, respectively), each dot represents the abundance of a tryptic peptide. For Collagen-I chains Col1a1 and Col1a2 have been grouped. For Collagen-VI, chains Col6a1, Col6a2 and Col6a3 have been grouped. ( E ) The ratio of semi-tryptic collagen-I peptide abundance compared to the average tryptic peptide abundance, this is as an indicator of degradation for Collagen-I and -VI in OA and RA. Each dot represents the ratio for a single semi-tryptic peptide. ( N = 12 for OA and 10 for RA). ( F ) Supporting data from RA synovial biopsy ( N = 8) dataset. Semi-tryptic ratio of collagen-I and –VI based on relevant spectral counts. Tryptic spectral counts ( G ) and semi-tryptic ratio ( H ) from the same dataset as ( F ) but separated into lymphoid ( N = 4) and myeloid ( N = 4) endotypes for grouped collagen-I and –VI. P values for t tests are labelled above each dot plot. ( I ) Dot plot of genes for type VI collagen chains and its processing regulators in each AMP1-like fibroblast cluster, split by disease activity status, coloured by scaled average expression, and sized by percentage of expressing cells. Red asterisks separate comparisons that led to genes being classified as DEGs. ( J ) Suggested mathematical model for out-of-phase oscillations in MMP2/MMP9 and TIMP3/TIMP4 expression, the subsequent anabolism potential of the tissue they induce, and its putative impact on collagen VI deposition. ( F : collagen I vs collagen VI in RA synovium P = 0.0011, G : lymphoid vs myeloid counts for collagen I P = 0.056 and for collagen VI P = 0.1056). Exact P values are given unless they are below 0.0001 which is beyond the calculation limit of the software used. .

Article Snippet: Rabbit anti-human COL1A1 , Cell Signalling Technologies , 28368S.

Techniques: Quantitative Proteomics, Activity Assay, Expressing, Software

Journal: Cancer biology & therapy

Article Title: Reprogramming of VEGF-mediated extracellular matrix changes through autocrine signaling.

doi: 10.1080/15384047.2023.2184145

Figure Lengend Snippet: Figure 3. Col1A1 immunostaining. (a) Representative images of Col1A1 immunostained tumor sections from viable (left) and necrotic (right) regions of 231_WT tumors. (b) Representative images of Col1A1 immunostained tumor sections from viable (left) and necrotic (right) regions of 231_VEGF tumors. Quantification of Col1A1 positive pixels normalized to the total pixel area of (c) viable tumor regions and (d) necrotic tumor regions from 231_WT (N = 5) and 231_VEGF (N = 5) tumors. Values represent Mean ± S.E.M. * P ≤ .05.

Article Snippet: Protein isolation and immunoblotting was performed as previously described.27 Antibodies cross-reactive with mouse/ human ECM proteins and specific for human enzymes of interest included rabbit-polyclonal anti-Col1A1 antibody (1:1000; OriGene, Rockville, MD, USA), mouse monoclonal anti-FN1 antibody (1:2000 dilution; Proteintech, Rosemont, IL, USA), rabbit polyclonal anti-MMP-1 antibody (1:1000 dilution; Neo BioLab, Woburn, MA, USA), rabbit polyclonal anti-MMP2 (1:1000 dilution; GeneTex, Inc., Irvine, CA, USA), rabbit polyclonal anti-MMP-14 antibody (1:1000 dilution; Neo BioLab, Woburn, MA, USA), mouse monoclonal anti-lysyl oxidase (LOX) antibody (1:1000 dilution; GeneTex, Inc., Irvine, CA, USA), mouse monoclonal anti-ADAMTS1 antibody (1:500 dilution; OriGene, Rockville, MD, USA), rabbit polyclonal anti-uPAR (1:1000 dilution; GeneTex, Inc., Irvine, CA, USA), mouse monoclonal anti-α-SMA antibody (1:2000; Novus Biologicals, Littleton, CO, USA), rabbit monoclonal antibody against neuropilin-1 (NRP-1) (1:1000, clone D62C6, Cell Signaling, Danvers, MA, USA, rabbit polyclone anti-FLT1 (VEGFR1) antibody (1:1000, MyBioSource, San Diego, CA) and rabbit polyclonal anti-FAP-α antibody (1:1000, Ab207178, Abcam, Cambridge, UK).

Techniques: Immunostaining

Journal: Cancer biology & therapy

Article Title: Reprogramming of VEGF-mediated extracellular matrix changes through autocrine signaling.

doi: 10.1080/15384047.2023.2184145

Figure Lengend Snippet: Figure 6. Immunoblot analysis of ECM proteins and enzymes in tumors. (a) Decrease of Col1A1 and fibronectin identified in 231_VEGF compared with 231_WT tumor samples. (b) Increase of MMP-1 in 231_VEGF compared with 231_WT tumor samples. (c) Decrease of MMP-2, and increase of uPAR in 231_VEGF compared with 231_WT tumor samples. (d) Decrease of ADAMST1 and (e) increase of LOX in 231_VEGF compared with 231_WT tumor samples. (f) Increase of α-SMA and decrease of FAP-α in 231_VEGF compared with 231_WT tumor samples. GAPDH was used as a loading control. n = 5 for 231_WT and n = 5 for 231_VEGF in all immunoblots.

Article Snippet: Protein isolation and immunoblotting was performed as previously described.27 Antibodies cross-reactive with mouse/ human ECM proteins and specific for human enzymes of interest included rabbit-polyclonal anti-Col1A1 antibody (1:1000; OriGene, Rockville, MD, USA), mouse monoclonal anti-FN1 antibody (1:2000 dilution; Proteintech, Rosemont, IL, USA), rabbit polyclonal anti-MMP-1 antibody (1:1000 dilution; Neo BioLab, Woburn, MA, USA), rabbit polyclonal anti-MMP2 (1:1000 dilution; GeneTex, Inc., Irvine, CA, USA), rabbit polyclonal anti-MMP-14 antibody (1:1000 dilution; Neo BioLab, Woburn, MA, USA), mouse monoclonal anti-lysyl oxidase (LOX) antibody (1:1000 dilution; GeneTex, Inc., Irvine, CA, USA), mouse monoclonal anti-ADAMTS1 antibody (1:500 dilution; OriGene, Rockville, MD, USA), rabbit polyclonal anti-uPAR (1:1000 dilution; GeneTex, Inc., Irvine, CA, USA), mouse monoclonal anti-α-SMA antibody (1:2000; Novus Biologicals, Littleton, CO, USA), rabbit monoclonal antibody against neuropilin-1 (NRP-1) (1:1000, clone D62C6, Cell Signaling, Danvers, MA, USA, rabbit polyclone anti-FLT1 (VEGFR1) antibody (1:1000, MyBioSource, San Diego, CA) and rabbit polyclonal anti-FAP-α antibody (1:1000, Ab207178, Abcam, Cambridge, UK).

Techniques: Western Blot, Control