Journal: Frontiers in Toxicology

Article Title: ICH S1 prospective evaluation study and weight of evidence assessments: commentary from industry representatives

doi: 10.3389/ftox.2024.1377990

Figure Lengend Snippet: Examples of Information sources ^a used in assessing target-related carcinogenic risk of small molecules.

Article Snippet: https://www.frontiersin.org/articles/10.3389/fgene.2022.1078050/full , Gene expression tissue atlas published by Abbvie scientists of nonclinical tox species - rat, mouse, dog, NHP.

Techniques: Expressing, Gene Expression, Transduction, Variant Assay, Mutagenesis

Journal: PLoS Computational Biology

Article Title: Digital Atlasing and Standardization in the Mouse Brain

doi: 10.1371/journal.pcbi.1001065

Figure Lengend Snippet: (a) WHS T1 MR image sliced on orthogonal planes. Color overlay on the planes represents segmentation of WHS anatomic regions. Blue-orange-yellow overlay is an ABA gene expression correlation map (from Anatomic Gene Expression Atlas [AGEA] online application, http://mouse.brain-map.org/agea ) rendered by maximum intensity projection and showing voxels where gene expression is highly correlated with the selected point of interest (POI). This POI, in the dentate gyrus of the hippocampus, was chosen in WHS, the coordinates transformed to ABA space, the corresponding correlation volume requested from the ABA Web service. The returned volume was finally transformed back to WHS for visualization. (b) Correlation volume in (a) merged with a volume rendering of WHS cropped around the hippocampus. (c) Surface representations of hippocampus in yellow and cortex in blue show the AGEA gene expression-defined dentate gyrus in relation to an MR-defined hippocampus. (d) Top four highest correlated genes from the ABA corresponding to (c). (e) A higher resolution view of the same query within the Allen Institute Brain Explorer interface.

Article Snippet: To illustrate the potential of the INCF Digital Atlasing framework, we integrated three major community resources into this developing infrastructure as atlas hubs: the ABA and associated tools such as the Anatomic Gene Expression Atlas (AGEA), EMAP/EMAGE for developmental mouse brain data, and the WBC, which integrates the UCSD/BIRN Smart Atlas (Spatial Mark-Up and Rendering Tool) and the Cell Centered Database (CCDB, http://www.ccdb.ucsd.edu/ ), including the Paxinos and Watson mouse brain atlas.

Techniques: Gene Expression, Transformation Assay

Journal: PLoS Computational Biology

Article Title: Digital Atlasing and Standardization in the Mouse Brain

doi: 10.1371/journal.pcbi.1001065

Figure Lengend Snippet: From the WBC 3-DAtlas Integration Client shown in (a), a user can generate a spatial query of WHS registered atlases. A probe can be placed in the 3-D space of the viewer and WHS coordinates of the probe translated into other atlas coordinate spaces. Implemented queries include (b) CCDB-UCSD, (c) EMAP/EMAGE, and (d) AGEA/ABA, enabling a framework for interchange between these atlases.

Article Snippet: To illustrate the potential of the INCF Digital Atlasing framework, we integrated three major community resources into this developing infrastructure as atlas hubs: the ABA and associated tools such as the Anatomic Gene Expression Atlas (AGEA), EMAP/EMAGE for developmental mouse brain data, and the WBC, which integrates the UCSD/BIRN Smart Atlas (Spatial Mark-Up and Rendering Tool) and the Cell Centered Database (CCDB, http://www.ccdb.ucsd.edu/ ), including the Paxinos and Watson mouse brain atlas.

Techniques:

Journal: Scientific reports

Article Title: Validating the role of PTGIS gene in colorectal cancer by bioinformatics analysis and in vitro experiments.

doi: 10.1038/s41598-023-43289-2

Figure Lengend Snippet: Figure 1. Expression and prognostic pattern of PTGIS in the pan-cancer perspective. (A) The expression of PTGIS from the perspective of pan-cancer; (B) in Oncomine database, the expression of PTGIS gene in tumor tissue is shown. The box shows the expression of PTGIS gene in colorectal cancer; (C) the prognosis of PTGIS from the perspective of pan-cancer.

Article Snippet: 6 Vol:. (1234567890) Scientific Reports | (2023) 13:16496 | https://doi.org/10.1038/s41598-023-43289-2 Figure 3. (A) The expression of PTGIS in colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues in Ualcan database; (B) the expression of PTGIS GEPIA 2 database of colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues; (C) q-PCR was used to detect the mRNA expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (D) WB was used to detect the protein expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (E) the protein levels of PTGIS based on Human Protein Atlas between Normal tissue and tumor tissue; (F) the relationship between PTGIS gene expression and prognosis in GEPIA 2 database; (G) objective to investigate the relationship between PTGIS gene expression and prognosis in LinkedOmics database.

Techniques: Expressing

Journal: Scientific reports

Article Title: Validating the role of PTGIS gene in colorectal cancer by bioinformatics analysis and in vitro experiments.

doi: 10.1038/s41598-023-43289-2

Figure Lengend Snippet: Figure 3. (A) The expression of PTGIS in colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues in Ualcan database; (B) the expression of PTGIS GEPIA 2 database of colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues; (C) q-PCR was used to detect the mRNA expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (D) WB was used to detect the protein expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (E) the protein levels of PTGIS based on Human Protein Atlas between Normal tissue and tumor tissue; (F) the relationship between PTGIS gene expression and prognosis in GEPIA 2 database; (G) objective to investigate the relationship between PTGIS gene expression and prognosis in LinkedOmics database.

Article Snippet: 6 Vol:. (1234567890) Scientific Reports | (2023) 13:16496 | https://doi.org/10.1038/s41598-023-43289-2 Figure 3. (A) The expression of PTGIS in colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues in Ualcan database; (B) the expression of PTGIS GEPIA 2 database of colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues; (C) q-PCR was used to detect the mRNA expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (D) WB was used to detect the protein expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (E) the protein levels of PTGIS based on Human Protein Atlas between Normal tissue and tumor tissue; (F) the relationship between PTGIS gene expression and prognosis in GEPIA 2 database; (G) objective to investigate the relationship between PTGIS gene expression and prognosis in LinkedOmics database.

Techniques: Expressing, Gene Expression

Journal: Scientific reports

Article Title: Validating the role of PTGIS gene in colorectal cancer by bioinformatics analysis and in vitro experiments.

doi: 10.1038/s41598-023-43289-2

Figure Lengend Snippet: Figure 6. Spearman correlation analysis between PTGIS gene and EMT pathway. X axis: represents the expression of genes, the Y axis: represents the pathway score.

Article Snippet: 6 Vol:. (1234567890) Scientific Reports | (2023) 13:16496 | https://doi.org/10.1038/s41598-023-43289-2 Figure 3. (A) The expression of PTGIS in colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues in Ualcan database; (B) the expression of PTGIS GEPIA 2 database of colon adenocarcinoma (COAD), rectal adenocarcinoma (read) and normal tissues; (C) q-PCR was used to detect the mRNA expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (D) WB was used to detect the protein expression of PTGIS in normal colorectal cells FHC, colorectal cancer cells SW480 and HCT8; (E) the protein levels of PTGIS based on Human Protein Atlas between Normal tissue and tumor tissue; (F) the relationship between PTGIS gene expression and prognosis in GEPIA 2 database; (G) objective to investigate the relationship between PTGIS gene expression and prognosis in LinkedOmics database.

Techniques: Expressing

Journal: International journal of cancer

Article Title: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth

doi: 10.1002/ijc.34564

Figure Lengend Snippet: (A) Left: LMVEC isolated from Ptprz1 +/+ and Ptprz1 −/− mice stained with rhodamine-conjugated Griffonia simplicifolia lectin as a marker of mouse endothelial cells or with an antibody specific for PTPRZ1 (red). Nuclei are stained with Draq5 (blue), and scale bars correspond to 10 μm. Right : Western blot analysis for PTPRZ1 in total protein extracts of Ptprz1 +/+ and Ptprz1 −/− LMVEC. Vinculin is used as a loading control. (B) Numbers of Ptprz1 −/− and Ptprz1 +/+ LMVEC at different time points after plating (mean ± SD, n=6). (C) Migration of Ptprz1 −/− and Ptprz1 +/+ LMVEC using the transwell assay (mean ± SD). (D) Representative photos and quantification of the tube network formed by Ptprz1 −/− and Ptprz1 +/+ LMVEC on Matrigel. Results are expressed as mean ± SD of the percent tube length compared to the Ptprz1 +/+ cells (set as default 100%). (E) LMVEC whole cell lysates were analyzed by antibodies against Akt phosphorylated at Ser473 (pAkt), total Akt (tAkt), ERK1/2 phosphorylated at Tyr895 (pERK1/2), and total ERK1/2 (tERK1/2). Representative Western blots are shown (n=3). Numbers denote the average fold change of the ratio pAkt/tAkt or pERK1/2/tERK1/2 compared to Ptprz1 +/+ LMVEC (set as default = 1). (F) Paraffin-embedded normal lung Ptprz1 −/− and Ptprz1 +/+ tissue sections stained with rhodamine-conjugated Griffonia simplicifolia lectin for endothelial cells (red). Nuclei are stained with Draq5 (blue). Representative pictures are shown, and the scale bar corresponds to 50 μm. Results are expressed as mean ± SD of the vascularized area per field of lung tissue in arbitrary units (AU).

Article Snippet: Our IHC data, as well as data from the Human Protein Atlas, show that PTPRZ1 gene expression in the adult lung is mostly restricted to the club and respiratory cells (Single cell type - PTPRZ1 - The Human Protein Atlas), which are important for chemically induced LUAD development [ 18 ]; our data suggest that the decreased PTPRZ1 expression enhances club cell transformation to LUAD cells.

Techniques: In Vitro, In Vivo, Isolation, Staining, Marker, Western Blot, Control, Migration, Transwell Assay

Journal: International journal of cancer

Article Title: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth

doi: 10.1002/ijc.34564

Figure Lengend Snippet: (A) Schematic representation of the experimental timeline. (B) Kaplan-Meier plot of Ptprz1 −/− and Ptprz1 +/+ mice survival. Statistical analysis was performed by using the Log-rank (Mantel-Cox) test. (C) Representative images of the lungs at the end of the experiment. Arrows indicate tumors. The number of tumors per lung (D) , tumor diameter and volume (E) , and total tumor burden per lung (F) are presented as mean ± SD. (G) Representative pictures from H&E-stained tumor tissue sections at 4x and 40x magnification. The arrows at 4x magnification point to tumors. Grading of urethane-induced tumors was estimated blindly on a scale from 1 to 5, with 1 indicating the lowest grade. (H) Representative pictures at 40x magnification of Ptprz1 −/− and Ptprz1 +/+ tumor tissue sections stained for PCNA (brown) and counterstained by hematoxylin (blue). Results are expressed as mean ± SD of the percent number of PCNA stained (PCNA + ) cells per field of tumor tissue. (I) Paraffin-embedded Ptprz1 −/− and Ptprz1 +/+ LUAD tissue sections stained for endothelial cells (red) and nuclei (blue). Representative pictures are shown, and the scale bar corresponds to 50 μm. Results are expressed as mean ± SD of the vascularized area per field of LUAD in arbitrary units (AU). (J) Representative pictures at 10x magnification of urethane-treated Ptprz1 −/− and Ptprz1 +/+ lung tissue sections stained for PTPRZ1 (brown) and counterstained by hematoxylin (blue). Ptprz1 −/− lungs were used as a negative control.

Article Snippet: Our IHC data, as well as data from the Human Protein Atlas, show that PTPRZ1 gene expression in the adult lung is mostly restricted to the club and respiratory cells (Single cell type - PTPRZ1 - The Human Protein Atlas), which are important for chemically induced LUAD development [ 18 ]; our data suggest that the decreased PTPRZ1 expression enhances club cell transformation to LUAD cells.

Techniques: In Vivo, Staining, Negative Control

Journal: International journal of cancer

Article Title: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth

doi: 10.1002/ijc.34564

Figure Lengend Snippet: (A) LMVEC whole cell lysates were analyzed by antibodies against β 3 integrin and vinculin (used as a loading control). Representative Western blots are shown (n=3). Numbers denote the average fold change of the ratio β 3 /vinculin compared to Ptprz1 +/+ LMVEC (set as default = 1). (B) LMVEC whole cell lysates following downregulation of β 3 by siRNA were analyzed using antibodies against β 3 integrin and β-actin. Representative Western blots are shown (n=3). Numbers denote the average fold change of the ratio β 3 /β-actin compared to the corresponding siNeg-treated LMVEC (set as default = 1). (C) Cell proliferation following downregulation of β 3 integrin. Results are expressed as mean ± SD of the percent number of cells compared to the corresponding control (set as default 100%). (D) Cell migration following downregulation of β 3 integrin. Results are expressed as mean ± SD. siNeg, cells transfected with a negative control siRNA; siβ 3 , cells transfected with siRNA for β 3 . (E) LMVEC whole cell lysates were analyzed by antibodies against c-Met and vinculin (used as a loading control). Representative Western blots are shown (n=3). Numbers denote the average fold change of the ratio c-Met/vinculin compared to Ptprz1 +/+ LMVEC (set as default = 1). (F) Formation of pTyr-c-Met complexes as evidenced by in situ PLA. Cells were incubated with crizotinib (1 μM) or the corresponding solvent for 2 h and then fixed and stained for tyrosine phosphorylated c-Met (pMet). Representative pictures are shown. The scale bar corresponds to 10 μm. The box plots indicate the median, mean, and range of the detected signals (n = 8-10 image fields with 3-6 cells per image per sample type, each sample run in triplicate). (G) Whole cell lysates of Ptprz1 +/+ and Ptprz1 −/− LMVEC cultured in the presence or absence of crizotinib were analyzed by antibodies against Akt phosphorylated at Ser473 (pAkt) and total Akt (tAkt). Representative Western blots are shown (n=3). Numbers denote the average fold change of the ratio pAkt/tAkt compared to untreated Ptprz1 +/+ LMVEC (set as default = 1). (H) Number of Ptprz1 +/+ and Ptprz1 −/− LMVEC cultured in the presence or absence of crizotinib (mean ± SD, n=3). Two-way ANOVA was used for statistical analysis. (I) Migration of Ptprz1 −/− and Ptprz1 +/+ LMVEC in the presence or absence of crizotinib (mean ± SD). (J) Representative photos and quantification of the tube network formed by Ptprz1 −/− and Ptprz1 +/+ LMVEC on Matrigel, in the presence or absence of crizotinib. Results are expressed as mean ± SD of the percent tube length compared to the solvent-treated Ptprz1 +/+ cells (set as default 100%).

Article Snippet: Our IHC data, as well as data from the Human Protein Atlas, show that PTPRZ1 gene expression in the adult lung is mostly restricted to the club and respiratory cells (Single cell type - PTPRZ1 - The Human Protein Atlas), which are important for chemically induced LUAD development [ 18 ]; our data suggest that the decreased PTPRZ1 expression enhances club cell transformation to LUAD cells.

Techniques: Expressing, Activation Assay, Migration, Control, Western Blot, Transfection, Negative Control, In Situ, Incubation, Solvent, Staining, Cell Culture

Journal: International journal of cancer

Article Title: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth

doi: 10.1002/ijc.34564

Figure Lengend Snippet: (A) Schematic representation of the experimental timeline. (B) Kaplan-Meier plot of the survival of the urethane-treated Ptprz1 −/− mice that received crizotinib or solvent. (C) Representative images of the lungs at the end of the experiment. Arrows indicate tumors. The number of tumors per lung (D), tumor diameter and volume (E), and total tumor burden per lung (F) are presented as mean ± SD. (G) Representative pictures at 40x magnification of Ptprz1 −/− and Ptprz1 +/+ tumor tissue sections stained for PCNA (brown) and counterstained by hematoxylin (blue). Results are expressed as mean ± SD of the percent number of PCNA stained (PCNA + ) cells per field of tumor tissue. (H) Representative pictures from H&E-stained tumor tissue sections at 10x and 40x magnification. The arrows at the 10x magnification point to tumors. Grading of urethane-induced tumors was estimated blindly on a scale from 1 to 5, with 1 indicating the lowest grade. (I) Tumors and adjacent normal Ptprz1 −/− and Ptprz1 +/+ lung tissue lysates from animals treated with crizotinib or solvent were analyzed using antibodies for Akt phosphorylated at Ser473 (pAkt) and total Akt (tAkt). Representative Western blots are shown (n=3). Numbers denote the average fold change of the ratio pAkt/tAkt compared with the adjacent normal Ptprz1 +/+ lung from mice treated with solvent (set as default = 1). (J) Paraffin-embedded LUAD tissue sections from animals treated with crizotinib or solvent are stained for tyrosine phosphorylated c-Met (red). Nuclei are stained with Draq5 (blue). Representative pictures are shown (n=3), and the scale bar corresponds to 50 μm. (K) Paraffin-embedded LUAD tissue sections from animals treated with crizotinib or solvent are stained for endothelial cells (red) and nuclei (blue). Representative pictures are shown, and the scale bar corresponds to 50 μm. Results are expressed as mean ± SD of vascularized area per field of LUAD in arbitrary units (AU).

Article Snippet: Our IHC data, as well as data from the Human Protein Atlas, show that PTPRZ1 gene expression in the adult lung is mostly restricted to the club and respiratory cells (Single cell type - PTPRZ1 - The Human Protein Atlas), which are important for chemically induced LUAD development [ 18 ]; our data suggest that the decreased PTPRZ1 expression enhances club cell transformation to LUAD cells.

Techniques: Solvent, Staining, Western Blot

Journal: International journal of cancer

Article Title: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth

doi: 10.1002/ijc.34564

Figure Lengend Snippet: (A) Numbers of Ptprz1 −/− and Ptprz1 +/+ LMVEC in the presence or absence of the PTPRZ1 TP inhibitor MY10 (10 μM) (mean ± SD, n=4). Two-way ANOVA was used for statistical analysis. (B) Migration of Ptprz1 −/− and Ptprz1 +/+ LMVEC in the presence or absence of MY10 (mean ± SD). (C) Representative photos and quantification of the tube network formed by Ptprz1 −/− and Ptprz1 +/+ LMVEC in the presence or absence of MY10 on Matrigel. Results are expressed as mean ± SD of the percent tube length compared to the solvent-treated Ptprz1 +/+ cells (set as default 100%). (D) The number of Ptprz1 +/+ LMVEC in the presence or absence of MY10 and/or crizotinib (1 μM) (mean ± SD, n=3). Two-way ANOVA was used for statistical analysis. (E) Migration of Ptprz1 +/+ LMVEC in the presence or absence of MY10 and/or crizotinib (mean ± SD). (F) Representative photos and quantification of the tube network formed by Ptprz1 +/+ LMVECs on Matrigel, in the presence or absence of MY10 and/or crizotinib. Results are expressed as mean ± SD (n=3) of the percent tube length compared to the solvent-treated Ptprz1 +/+ cells (set as default 100%). (G) Formation of tyrosine phosphorylated c-Met (pMet) complexes as evidenced by in situ PLA in Ptprz1 +/+ LMVECs cultured in the presence or absence of MY10 and crizotinib. Representative pictures are shown. The scale bar corresponds to 10 μm. The box plots indicate the median, mean, and range of the detected signals (n = 8-10 image fields with 4-6 cells per image per sample type, each sample run in triplicate).

Article Snippet: Our IHC data, as well as data from the Human Protein Atlas, show that PTPRZ1 gene expression in the adult lung is mostly restricted to the club and respiratory cells (Single cell type - PTPRZ1 - The Human Protein Atlas), which are important for chemically induced LUAD development [ 18 ]; our data suggest that the decreased PTPRZ1 expression enhances club cell transformation to LUAD cells.

Techniques: Migration, Solvent, In Situ, Cell Culture

Journal: International journal of cancer

Article Title: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth

doi: 10.1002/ijc.34564

Figure Lengend Snippet: (A) Formation of tyrosine phosphorylated c-Met (pMet) complexes as evidenced by in situ PLA in HUVEC cultured in the presence or absence of VEGFA 165 (10 ng/ml). Representative pictures are shown. The scale bar corresponds to 10 μm. The box plots indicate the median, mean, and range of the detected signals (n = 8-10 image fields with 4-8 cells per image per sample type, each sample run in triplicate). (B) Number of HUVEC in the presence or absence of VEGFA 165 and/or crizotinib (1 μM) for 24 h (mean ± SD). (C) Migration of HUVEC in the presence or absence of VEGFA 165 and/or crizotinib. Results are expressed as mean ± SD of the percent number of migrated cells compared to the solvent-treated cells (set as default 100%). (D) HUVEC were treated with VEGFA 165 and/or crizotinib and cell lysates were analyzed by antibodies against Akt phosphorylated at Ser473 (pAkt), and total Akt (tAkt). A representative Western blot is shown (n=3). Numbers denote the average fold change of the ratio pAkt/tAkt compared to untreated HUVEC (set as default = 1). (E) Formation of tyrosine phosphorylated c-Met (pMet) complexes as evidenced by in situ PLA in HUVEC cultured in the presence or absence of PTN (100 ng/ml). Representative pictures are shown. The scale bar corresponds to 10 μm. The box plots indicate the median, mean, and range of the detected signals (n = 8-10 image fields with 4-8 cells per image per sample type, each sample run in triplicate). (F) Migration of HUVEC in the presence or absence of PTN and/or crizotinib. Results are expressed as mean ± SD of the percent number of migrated cells compared to the solvent-treated cells (set as default 100%). (G) Migration of Ptprz1 −/− and Ptprz1 +/+ LMVEC in the presence or absence of VEGFA 165 or PTN (mean ± SD). (H) Migration of HUVEC in the presence or absence of MY10, stimulated by VEGFA 165 or PTN. Results are expressed as mean ± SD of the percent number of migrated cells compared to the solvent-treated cells (set as default 100%). (I) Schematic presentation of the pathway activated by PTPRZ1 deficiency or inhibition in endothelial cells and LUAD. Deficient PTPRZ1 expression results in β 3 integrin downregulation and activation of c-Met and Akt in endothelial and LUAD cells, leading to activation of endothelial cells, angiogenesis, and LUAD growth (left). VEGFA, PTN, and a specific PTPRZ1 TP inhibitor (MY10) also activate c-Met and Akt in endothelial cells (right). Crizotinib abolishes both LUAD growth and angiogenesis due to low PTPRZ1 expression levels, and the stimulatory effects of VEGFA, PTN, and MY10 on endothelial cell activation. The figure was created with Biorender.

Article Snippet: Our IHC data, as well as data from the Human Protein Atlas, show that PTPRZ1 gene expression in the adult lung is mostly restricted to the club and respiratory cells (Single cell type - PTPRZ1 - The Human Protein Atlas), which are important for chemically induced LUAD development [ 18 ]; our data suggest that the decreased PTPRZ1 expression enhances club cell transformation to LUAD cells.

Techniques: In Situ, Cell Culture, Migration, Solvent, Western Blot, Inhibition, Expressing, Activation Assay