Journal: Frontiers in Immunology

Article Title: ULK1 Inhibition as a Targeted Therapeutic Strategy for Psoriasis by Regulating Keratinocytes and Their Crosstalk With Neutrophils

doi: 10.3389/fimmu.2021.714274

Figure Lengend Snippet: Inhibition of ULK1 suppresses proliferation and promotes apoptosis of keratinocytes in vitro . (A) Immunoblot of HaCat keratinocytes 24 hours after cocultured with DMSO, 5 µM or 10 µM SBI-0206965 (SBI). (B) Cell cycle analysis of HaCat keratinocytes treated with DMSO or 10 µM SBI for 24 hours. The bar graph shows the percentage of cell population in each phase of cell cycle. (C) Apoptosis of HaCat keratinocytes 24 hours after serum deprivation in the presence of DMSO or 10 µM SBI. (D) mRNA expression of psoriasis-related inflammatory mediators in HaCat keratinocytes cocultured with DMSO or 10 µM SBI for 24 hours. (E) mRNA and protein expression of ULK1 in HaCat keratinocytes transfected with negative control-siRNA(NC-siRNA) and ULK1-siRNA. (F) Cell cycle analysis of HaCat keratinocytes 72 hours after transfection with NC-siRNA or ULK1-siRNA. (G) Apoptosis of transfected HaCat keratinocytes 24 hours after serum deprivation. (H) mRNA expression of psoriasis-related inflammatory mediators in HaCat keratinocytes transfected with NC-siRNA or ULK1-siRNA for 72 hours. Data are presented as mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001.

Article Snippet: Primary keratinocytes (PCS-200-010, ATCC) were cultured in Dermal Cell Basall Medium (PCS-200-030, ATCC) supplemented with Keratinocyte Growth Kit (PCS-200-040, ATCC), 10U/mL of penicillin and 10μg/mL of streptomycin and 25ng/mL of amphotericin (03-033-1B, BI).

Techniques: Inhibition, In Vitro, Western Blot, Cell Cycle Assay, Expressing, Transfection, Negative Control

Journal: Frontiers in Immunology

Article Title: ULK1 Inhibition as a Targeted Therapeutic Strategy for Psoriasis by Regulating Keratinocytes and Their Crosstalk With Neutrophils

doi: 10.3389/fimmu.2021.714274

Figure Lengend Snippet: Inactivation of ULK1 by SBI suppressed the inflammation in keratinocytes stimulated by neutrophil. (A) mRNA expression of psoriasis-related inflammatory mediators by keratinocytes stimulated with neutrophils isolated from healthy donors (HC) or (B) psoriasis patients in the presence of 10 µM DMSO or SBI for 10 hours. Data are representative of three independent experiments. Data are presented as mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

Article Snippet: Primary keratinocytes (PCS-200-010, ATCC) were cultured in Dermal Cell Basall Medium (PCS-200-030, ATCC) supplemented with Keratinocyte Growth Kit (PCS-200-040, ATCC), 10U/mL of penicillin and 10μg/mL of streptomycin and 25ng/mL of amphotericin (03-033-1B, BI).

Techniques: Expressing, Isolation

Journal: Frontiers in Immunology

Article Title: ULK1 Inhibition as a Targeted Therapeutic Strategy for Psoriasis by Regulating Keratinocytes and Their Crosstalk With Neutrophils

doi: 10.3389/fimmu.2021.714274

Figure Lengend Snippet: Autophagy inhibitors fail to fully replicate the effect of ULK1 inhibition on keratinocyte. (A–C) Expression of p62 and LC3 I/II in HaCat keratinocytes 24 hours after incubation with SBI0206965 (SBI) (A) or chloroquine (B) or 3-methyladenine(3-MA) at indicated concentration (C) . (D) Cell cycle analysis and (E) apoptosis of keratinocytes after 24 hours with the treatment of 10 µM chloroquine or 5 mM 3-MA. (F) mRNA expression of psoriasis-related inflammatory mediators by keratinocytes cocultured with neutrophils from healthy donors in the presence of 5 mM 3-MA. Data are representative of three independent experiments. Data are presented as mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

Article Snippet: Primary keratinocytes (PCS-200-010, ATCC) were cultured in Dermal Cell Basall Medium (PCS-200-030, ATCC) supplemented with Keratinocyte Growth Kit (PCS-200-040, ATCC), 10U/mL of penicillin and 10μg/mL of streptomycin and 25ng/mL of amphotericin (03-033-1B, BI).

Techniques: Inhibition, Expressing, Incubation, Concentration Assay, Cell Cycle Assay

Journal: Orphanet Journal of Rare Diseases

Article Title: Molecular diagnosis of anti-laminin 332 (epiligrin) mucous membrane pemphigoid

doi: 10.1186/s13023-018-0855-x

Figure Lengend Snippet: Detection of autoantibodies by ELISA with extracellular matrix of cultured keratinocytes. The extracellular matrix was obtained by treatment of cultured HaCaT keratinocytes with 20 mM NH4OH as detailed in Methods. a SDS-PAGE analysis of the extracellular matrix extract shows the migration of laminin 332 chains (arrows) at about 165 kDa (α3 chain), 140 kDa (β3 chain) as well as 155 kDa and 105 kDa (unprocessed and processed forms of the γ2 chain). b Immunoreactivity of mucous membrane pemphigoid autoantibodies with the laminin 332 from the extracellular matrix extract. Extracellular matrix extract was electrophoretically separated by 8% SDS-PAGE, transferred to nitrocellulose and immunoblotted with rabbit anti-human laminin 332 polyclonal antibody (lane 1), anti-laminin 332 mucous membrane pemphigoid patient’s sera (lanes 2–4), normal human sera (lane 5), and normal rabbit sera (lane 6). c Receiver-operating-characteristic (ROC) curve. AUC, area under the curve. Test performed with sera from patients with confirmed anti-laminin 332 mucous membrane pemphigoid ( n = 36) and controls ( n = 116). d ELISA reactivity of human sera with extracellular matrix. Scatter plots represent optical density measurements of serum reactivity from patients with mucous membrane pemphigoid (MMP; n = 36) with confirmed laminin 332-specific autoantibodies, MMP patients with possible laminin 332-specific autoantibodies ( n = 30), from healthy donors (NHS; n = 116), as well as from patients with bullous pemphigoid (BP; n = 89), pemphigus vulgaris (PV; n = 49), epidermolysis bullosa acquisita (EBA; n = 19), and dermatitis herpetiformis (DH; n = 41). The cut-off of the assay is represented by a dotted line (cut-off = 0.367, sensitivity = 83.33%, specificity = 84.48%)

Article Snippet: Native commercially available laminin 332 purified by affinity chromatography from cell culture supernatant of human foreskin keratinocytes has been purchased from Immundiagnostik.

Techniques: Enzyme-linked Immunosorbent Assay, Cell Culture, SDS Page, Migration

Journal: Orphanet Journal of Rare Diseases

Article Title: Molecular diagnosis of anti-laminin 332 (epiligrin) mucous membrane pemphigoid

doi: 10.1186/s13023-018-0855-x

Figure Lengend Snippet: Use of laminin 332-specific immunoassays in the diagnostic algorithm in mucous membrane pemphigoid. The ELISA with extracellular matrix could represent an addition in patients with a high index of clinical suspicion of mucous membrane pemphigoid showing compatible results by direct immunofluorescence microscopy and either negative or positive findings with dermal binding by indirect immunofluorescence microscopy. A positive result by ELISA with keratinocyte extracellular matrix should be subsequently confirmed by immunoblotting

Article Snippet: Native commercially available laminin 332 purified by affinity chromatography from cell culture supernatant of human foreskin keratinocytes has been purchased from Immundiagnostik.

Techniques: Diagnostic Assay, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Microscopy, Binding Assay, Western Blot

Journal: The Journal of Cell Biology

Article Title: Actinin-4, a Novel Actin-bundling Protein Associated with Cell Motility and Cancer Invasion

doi:

Figure Lengend Snippet: Detection of actinin-4 protein and mRNA. ( A ) Immunoblot analysis of actinin-4 in HFK and various human cancer cell lines with mAb NCC-Lu-632. Actinin-4 protein was detected in cell lysates from HFK (lane 1 ), lung cancer cell lines Lu-65 (lane 2 ) and PC-10 (lane 3 ), vulvar cancer cell line A-431 (lane 4 ), and esophageal cancer cell lines TE 4 (lane 5 ), TE 6 (lane 6 ), TE 7 (lane 7 ), TE 10 (lane 8 ), and TE 11 (lane 9 ). Molecular masses (in kD) are shown on the left. ( B ) Expression of actinin-4 mRNA in normal human tissues. Human multiple tissue Northern blots I and II (CLONTECH Laboratories) were hybridized with an actinin-4–specific oligonucleotide. Each lane contains 2 μg of poly(A) + RNA of human adult tissues: heart (lane 1 ), brain (lane 2 ), placenta (lane 3 ), lung (lane 4 ), liver (lane 5 ), skeletal muscle (lane 6 ), kidney (lane 7 ), pancreas (lane 8 ), spleen (lane 9 ), thymus (lane 10 ), prostate (lane 11 ), testis (lane 12 ), ovary (lane 13 ), small intestine (lane 14 ), colon (lane 15 ), and peripheral blood leukocytes (lane 16 ). Molecular masses (in kb) are shown on the left side.

Article Snippet: Primary cultured human foreskin keratinocytes (HFK) 1 were purchased from Seikagaku Co. (Tokyo, Japan) and were cultured as instructed by the supplier.

Techniques: Western Blot, Expressing, Northern Blot

Journal: The Journal of Cell Biology

Article Title: Actinin-4, a Novel Actin-bundling Protein Associated with Cell Motility and Cancer Invasion

doi:

Figure Lengend Snippet: Immunofluorescence microscopy showing translocation of actinin-4 protein from the cytoplasm to the nucleus. ( A ) In control untreated HFK, actinin-4 was found to exist in the cytoplasm. ( B ) After treatment of HFK with wortmannin, actinin-4 protein was translocated into the nucleus. Bar, 5 μm.

Article Snippet: Primary cultured human foreskin keratinocytes (HFK) 1 were purchased from Seikagaku Co. (Tokyo, Japan) and were cultured as instructed by the supplier.

Techniques: Immunofluorescence, Microscopy, Translocation Assay, Control

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A Immunoblots: 4OHT dose–response of ER:HRas G12V induction. The activity of HRas G12V was monitored by a RAS-GTP-binding assay, which leads to downstream activation of P-ERK and P-Akt. B Immunoblots comparing ER:HRas G12V levels between supplemented (5 ng/mL of EGF and 5 µL/mL of pituitary extract) and nonsupplemented media in ER:HRas G12V -keratinocyte cultures. The immunoblot of cells in the supplemented medium is a projection of the one presented in A . The electrophoresis gel of cell lysates derived from cells grown in either supplemented or nonsupplemented media, was blotted in the same membrane to allow comparison of ER:HRas G12V levels and HRas G12V -GTP (HRas G12V -GTP = HRas G12V activity) under both conditions. C Growth curves of ER:HRas G12V keratinocytes in function of 4OHT concentration. The graph is representative of three independent experiments carried out in duplicate. D Effect of 50 nM 4OHT in ER:HRas G12V keratocytes growing in supplemented or nonsupplemented media. The graph is representative of three independent experiments carried out in duplicate. E Evolution of the sub-G1 population of ER:HRas G12V keratocytes growing in complete medium induced or not with 50 nM of 40HT, measured by flow cytometry after PI staining. The graph is representative of two independent experiments. For flow cytometry, 30 × 10 3 events were considered per condition and time point. Growth curves and the sub-G1 population are presenting data as mean (SD). Two-way ANOVA *P ≤ 0.05, ** P ≤ 0.01, and *** P ≤ 0.001, Bonferroni post hoc.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: Western Blot, Activity Assay, GTP Binding Assay, Activation Assay, Electrophoresis, Derivative Assay, Membrane, Comparison, Concentration Assay, Flow Cytometry, Staining

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A Growth curve of ER:HRas G12V keratinocytes in the supplemented medium induced or not with 50 nM of 4OHT. The graph is representative of three independent experiments carried out in triplicate. B Cell cycle profile analyses of growing ER:HRas G12V keratinocytes, using 1-h pulse of EdU incorporation and propidium iodide (PI) staining, showed a progressive decrease in DNA synthesis (red arrows) in cells induced with 50 nM 4OHT. C DNA content profiles of growing ER:HRas G12V keratinocytes stained with PI, with or without 4OHT induction. D Steady-state growing ER:HRas G12V keratinocytes were induced or not with 50 nM 4OHT at zero time: kinetics of the relative size of cell cycle-phase subpopulations; evidence of cell cycle arrest at G1/G0 and G2/M phases only in 4OHT-induced cells. The graph is representative of four independent experiments, two PI single-labeled, and two PI plus EdU double-labeled. All conditions and time points were carried out in duplicate. E Immunoblots showed intracellular levels of critical components of cell cycle control pathways in growing ER:HRas G12V keratinocytes induced or not with 4OHT. For flow cytometry, 30 × 10 3 cells were considered per condition and time point. Data presented as a mean (SD). Two-way ANOVA * P ≤ 0.05, ** P ≤ 0.01, and *** P ≤ 0.001, Bonferroni post hoc.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: Staining, DNA Synthesis, Labeling, Western Blot, Control, Flow Cytometry

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A TUNEL assays showed high levels of DNA strand breaks (DSB) in cells after six days of 4OHT induction in a dose-dependent manner. Two groups of controls were used: noninduced ER:HRas G12V keratinocytes and ER:ø-keratinocytes treated with 50 nM of 4OHT emphasizing that the increasing levels of HRas G12V , but not 4OHT, are responsible for DNA breaks, n = 100 cells per condition. The whole experiment (including the experimental controls and the other 4OHT concentrations used), is presented in Supplementary Fig. S . B In ER:HRas G12V keratinocytes, native chromatin-BrdU assay showed persistent sites of single-stranded DNA (ssDNA) after six days of 50 nM 4OHT induction. For each condition and day analyzed, at least 50 nuclei were counted and classified into three different phenotypes: normal ≤10 foci/nucleus, the initial stage of replication stress ≥10 ≤ 50 foci/nucleus, and advanced stage of replication stress ≥50 foci/nucleus. The whole kinetic experiment is displayed in Supplementary Fig. S . C Sub-G1 populations increased with dose and time of HRas G12V induction. The graph is representative of two independent experiments carried out in duplicate. D Annexin-V/PI-flow cytometry analyses: ER:HRas G12V keratinocytes induced with 50 nM of 4OHT and the noninduced control condition were analyzed for 10 days. Density plots are presented as an example of the profile of ER:HRas G12V keratinocytes in days 6 and 8. E In the same kinetic design, the treatment with 25 µM of the caspase inhibitor ZVAD did not rescue the viability of keratinocytes under high HRas G12V activity. The graphs are representative of three independent experiments. For flow cytometry, 30 × 10 3 cells were considered per condition and time point. Data presented as a mean (SD). One-way ANOVA for B and two-way ANOVA for C and D. * P ≤ 0.05, ** P ≤ 0.01, and *** P ≤ 0.001, Bonferroni post hoc.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: TUNEL Assay, BrdU Staining, Flow Cytometry, Control, Activity Assay

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A Immunoblots of ER:HRas G12V keratinocytes induced for 48 h with 50 nM 4OHT, treated or not with 5 mM of NAC. B Growth curves of ER:HRas G12V keratinocyte induced or not, showing the protective effect of NAC on cell proliferation. The graph is representative of two independent experiments carried out in duplicate. C DNA content by PI-flow cytometry analyses showed that NAC increased cell viability, evidenced by the elimination of the sub-G1 population on the 8th day of induction. The graph is representative of two independent experiments. D Annexin-V/PI-flow cytometry cell viability assays: quantified density plot graphs also demonstrated NAC survival effect on ER:HRas G12V keratinocytes induced with 4OHT. Density plots are presenting the profile of keratinocytes treated or not with 4OHT on their 8th day. The graph is representative of two independent experiments. E PI-flow cytometry cell cycle analyses showed that NAC-treated ER:HRas G12V keratinocytes could overcome the G1 and G2/M cell cycle arrest caused by high HRas G12V activity. The significance presented in the graph is related to the comparison between cells induced with 50 nM of 4OHT with (dark green) or without (gray) NAC treatment. The graph is representative of two independent experiments. For flow cytometry, 30 × 10 3 cells were considered per condition and time point. Data presented as mean (SD). Two-way ANOVA * P ≤ 0.05, ** P ≤ 0.01, and *** P ≤ 0.001, Bonferroni post hoc.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: Western Blot, Flow Cytometry, Activity Assay, Comparison

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A Immunoblots of ER:HRas G12V keratinocytes presenting autophagy markers (LC3II and p62) under 48 h of CQ (5 µM) treatment induced or not with 4OHT (50 nM). B The growth curve of induced ER:HRas G12V keratinocytes suggests loss of cell viability of keratinocytes that had their autophagy flux inhibited. The graph is representative of three independent experiments carried out in duplicate per condition and time point. C DNA content analysis by flow cytometry using PI of labeled ER:HRas G12V keratinocytes showed a drastic increase of sub-G1 population in 4OHT-induced keratinocytes treated with CQ. The graph is representative of two independent experiments. D Immunoblots of ER:HRas G12V autophagy-defective keratinocytes (ΔATG7 keratinocytes) and their control autophagy-competent scrabble (Scrb keratinocytes). The absence of ATG7 and LC3II in ΔATG7 keratinocytes induced with 50 nM 4OHT confirmed successful knockout of the ATG7 gene and ablation of the autophagy pathway. E Growth curves using different 4OHT concentrations and consequently different levels of HRas G12V activity. The graph is representative of three independent experiments carried out in duplicate. F Flow cytometry of cell viability assay stained with annexin-V/PI. Density plot graphs (8th day) and their quantification indicate that autophagy activity is crucial for keratinocyte survival under oncogenic stress promoted by HRas G12V activity. The graph is representative of two independent experiments in which 30 × 10 3 cells were considered per condition and time point. Data presented as a mean (SD). Two-way ANOVA, * P ≤ 0.05, ** P ≤ 0.01, and *** P ≤ 0.001, Bonferroni post hoc.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: Western Blot, Flow Cytometry, Labeling, Control, Knock-Out, Activity Assay, Viability Assay, Staining

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A Flow cytometry measurements of reactive oxygen species (ROS) through DCF fluorescence. Autophagy-competent (Scrb keratinocytes I–III) and autophagy-deficient keratinocytes (ΔATG7 keratinocytes II–IV) were induced with 50 nM 4OHT and treated with 5 mM NAC for 48 h (I, II) or 96 h (III, IV). The red brackets show the gradual increase in ROS levels in autophagy-competent cells and the fast increase of ROS levels in keratinocytes lacking autophagy. B ΔATG7 keratinocytes increase in 70% of their ROS levels after 48 h of HRas G12V induction. The levels in autophagy-competent keratinocytes were much lower (20%). In addition, NAC treatment reduced steady-state levels of ROS in noninduced keratinocytes. The dislocation of the fluorescent population was quantified by the Kolmogorov–Smirnov test (K–S). The graphs are representative of three independent experiments. C The conditioned culture media of ER:HRas G12V keratinocytes, 4OHT-induced and noninduced (control), were harvested for 10 days and had their lactate concentration measured. The graph is representative of two independent experiments carried out in triplicate. D The flow cytometry of cell viability assay stained with annexin-V/PI showed that deoxynucleoside treatment improved keratinocytes’ survival under oncogenic stress promoted by HRas G12V activity. The ER:HRas G12V keratinocytes were plated in lower density to extend as much as possible the experiment. After 6 days, the cells were induced with 50 nM 4OHT, treated with 2 mM deoxynucleosides (deoxyadenine, -guanosine, -cytidine, and thymidine) and their respective controls had their viability measured. The graph is representative of two independent experiments. The different font sizes represent the intensity of the effect. For flow cytometry, 30 × 10 3 cells were considered per condition and time point. Data presented as a mean (SD). Two-way ANOVA, * P ≤ 0.05, ** P ≤ 0.01, and *** P ≤ 0.001, Bonferroni post hoc.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: Flow Cytometry, Fluorescence, Control, Concentration Assay, Viability Assay, Staining, Activity Assay

Journal: Cell Death & Disease

Article Title: Autophagy buffers Ras-induced genotoxic stress enabling malignant transformation in keratinocytes primed by human papillomavirus

doi: 10.1038/s41419-021-03476-3

Figure Lengend Snippet: A Step-by-step of the models generated and the role of HRas G12V activity in their fates. Note that the different levels of inducible ER:HRas G12V activity are mimicking the fates observed in the constitutive ones. In the constitutive model, we could observe only the product of a random selection of cells presenting low levels of HRas G12V activity. Nonetheless, using the inducible model, we were able to observe the phenomenon responsible for such selection. B Mechanistic model presenting the challenge that HPV-primed keratinocytes, in the transition to a malignant transformed phenotype, must bypass according to the intensity of oncogenic stress (ROS, imbalanced metabolism, replication stress, and DNA damage). The intensity of the oncogenic stress is determined by different levels of HRas G12V activity and it is counterbalanced by autophagic activity in a different fashion: (I) only a moderate level of HRas G12V activity is supported by immortalized E6E7 keratinocytes since the autophagy activity, also moderate, is capable of buffering the oncogenic stress generated. (II) However, without the recruitment of autophagy, any level of oncogenic stress is not tolerated, proving that autophagy is recruited primarily as a safeguard mechanism. (III) On the other hand, high levels of HRas G12V activity generate unbearable oncogenic stress followed by the activation of autophagy over the cell capacity of processing that becomes an additional source of stress leading to cell death. The different font sizes are expressing the levels of cell signaling/events observed.

Article Snippet: Primary foreskin human keratinocytes (PHK) (Lonza Walkersville, Inc., Walkersville, MD) were transduced with pLXSN-encoding E6E7–HPV16 proteins.

Techniques: Generated, Activity Assay, Selection, Transformation Assay, Activation Assay, Expressing

Journal: Pharmaceuticals

Article Title: Predicting the Skin Sensitization Potential of Small Molecules with Machine Learning Models Trained on Biologically Meaningful Descriptors

doi: 10.3390/ph14080790

Figure Lengend Snippet: Overview of the Top-10 Bioactivity Descriptors.

Article Snippet: p0 BSK KF3CT ICAM1 down , Bioseek human keratinocytes and foreskin fibroblasts intercellular adhesion molecule 1 assay , 0.074 , 0.009 , positive , 0.80 , 0.83 , 0.41 , BSK KF3CT SRB down (0.79).

Techniques: Mutagenesis, Activity Assay, Activation Assay, Luciferase