rabbit polyclonal anti phosphorylated p38 thr180 tyr182  (Cell Signaling Technology Inc)

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: p38 is activated in progenitors after P.e. infection (A-D) . Phosphorylated-p38 (p-p38) (A, B: red; A’, B’: LUT) levels increase throughout the midgut epithelium including the progenitors (GFP in A, B; green-dashed outline in A-B’) in P.e. infected midguts compared to uninfected control midguts. The distribution (histogram) of p-p38 fluorescence intensity per progenitor from control uninfected midguts (n=5 midguts from one of two experiments) and P.e. -infected midguts (n=4 midguts from one of two experiments) (C). The mean p-p38 fluorescence intensity in progenitors per midgut with mean and 95% CI are shown for control midguts (n=5 from one of two experiments) and P.e .-infected control midguts (n = 4 from one of two experiments) (Mann–Whitney; p-value = 0.0159) (D). p38 is required in ISCs for their proliferation (E-F) . Depleting p38a and p38b in progenitors with esg ts and in ISCs with esg ts Su(H)Gal80 for 4 days blocks ISC proliferation by 73.4% (Mann–Whitney; p < 0.0001) and 59.6% (Mann–Whitney; p < 0.0001), respectively, compared to P.e. -infected control midguts. The mean number of PH3-positive cells per midgut with 95% CI is shown for control midguts (n = 21 pooled from three experiments), P.e. infected control midguts (n = 22 pooled from three experiments), midguts expressing p38a+b RNAi (1) in progenitors for 4 days (n = 26 pooled from three experiments) and P.e. -infected guts expressing p38a+b RNAi (1) in progenitors for 4 days (n = 34 pooled from three experiments) (E). The mean number of PH3-positive cells per midgut with 95% CI in control midguts (n = 18 pooled from two experiments), P.e. -infected control midguts (n = 21 pooled from two experiments), midguts expressing p38a+b RNAi (1) in ISCs for 4 days (n = 15 pooled from two experiments) and P.e. -infected midguts expressing p38a+b RNAi (1) in ISCs for 4 days (n = 18 pooled from two experiments) (F). In E and F, the mean number of mitoses per midgut increased in P.e.- infected control midguts compared to uninfected midguts (Mann-Whitney; p<0.0001). p38 is required in progenitors for p38 activation throughout the midgut epithelium after P.e. infection (G) . p38 fluorescent intensity significantly increases throughout the midgut epithelium after P.e. infection. Depletion of either p38a and p38b or p38b alone in progenitors with esg ts for 4 days reduces p38 activation throughout the midgut epithelium after P.e. infection by 102.1% (Mann-Whitney; p value = 0.0079) and 62.9% (Mann-Whitney; p-value = 0.0079), respectively, compared to control infected midguts. The mean fluorescence intensity for epithelial p38 is shown for control midguts (n = 5 from one experiment), P.e. -infected control midguts (n = 5 from one experiment), midguts expressing p38a+b RNAi (2) in progenitors (n = 5 from one experiment) and P.e. -infected midguts expressing p38a+b RNAi (2) in progenitors (n = 5 from one experiment). The mean fluorescence intensity for epithelial p38 increased in P.e.- infected control midguts compared to uninfected midguts (Mann-Whitney; p-value = 0.0079) (G). Scale bars are 30μm.

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Infection, Control, Fluorescence, MANN-WHITNEY, Expressing, Activation Assay

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: Licorne overexpression in progenitors activates p38 in progenitors and in nearby midgut epithelial cells (A-C) . Phosphorylated-p38 (p-p38) (A, B: red; A’, B’: LUT) increases in midgut progenitors (A, B: GFP; A-B’, green-dashed outline) and in nearby epithelial cells after overexpressing licorne with esg ts compared to control midguts. The distribution (histogram) of p-p38 fluorescence intensity per progenitor is shown for control midguts (n=5 from one experiment) and midguts overexpressing licorne in progenitors for 1 day with esg ts (n=5 from one experiment). Licorne overexpression in midguts promotes ISC proliferation (C) . The mean number of PH3-positive cells per midgut with 95% CI increases in midguts overexpressing licorne in progenitors for 1 day (n = 24 from one experiment) compared to control midguts (n = 19 from one experiment) (Mann–Whitney; p < 0.0001) (D). Scale bars are 30μm.

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Over Expression, Control, Fluorescence, MANN-WHITNEY

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: Licorne is required in progenitors for ISC proliferation after P.e. infection (A). Depleting licorne by expressing licorne RNAi (1) in progenitors for 4 days with esg ts suppresses ISC proliferation by 97.7% compared to control P.e. -infected midguts (Mann–Whitney; p < 0.0001) (A). The mean number of PH3-positive cells per midgut with mean and 95% CI are shown for control midguts (n = 21 from one experiment), P.e. -infected control midguts (n = 20 from one experiment), midguts expressing licorne RNAi (1) in progenitor cells for 4 days (n = 17 from one experiment) and P.e.- infected midguts expressing licorne RNAi (1) in progenitors for 4 days (n = 18 from one experiment) (A). In A, the mean number of mitoses per midgut increased in P.e.- infected control midguts compared to uninfected control midguts (Mann-Whitney; p<0.0001). Licorne is required in progenitors for p38 activation in progenitors and throughout the midgut epithelium after P.e. infection (B-K) . p38 activation is blocked in progenitors and throughout the midgut epithelium of P.e. -infected midguts expressing licorne RNAi (1) in progenitors by 87.5% (Mann-Whitney; p-value = 0.0087) and 73.9% (Mann-Whitney; p-value = 0.0260), respectively, compared to control P.e. -infected midguts (B-C). In B, the mean p-p38 fluorescent intensity in progenitors per midgut with mean and 95% CI are shown for control midguts (n = 6 from one experiment), P.e. -infected control midguts (n = 6 from one experiment), midguts expressing licorne RNAi (1) in progenitors for 4 days (n = 6 from one experiment) and P.e. -infected midguts expressing licorne RNAi (1) in progenitors for 4 days (n = 6 from one experiment). In C, the epithelial p- p38 fluorescence intensity per midgut (from those analysed in B) are shown with mean and 95%CI. In B and C, the mean p-p38 fluorescence intensity increased in P.e.- infected control midguts compared to uninfected control midguts (Mann-Whitney; p value = 0.0043 in B; Mann-Whitney; p-value = 0.0022 in C). p-p38 (D, E: red; D’, E’: LUT) increases in progenitors (E: GFP; E-E’: green-dashed outline) and throughout the midgut epithelium after P.e. infection compared to control (D-D’). Depleting licorne from progenitors for 5 days blocks the increase in p-p38 in progenitors and throughout the midgut epithelium (G-G’) compared to P.e .-infected control midguts (E-E’). The distribution (histogram) of p-p38 fluorescence intensity per progenitor is shown for uninfected control midguts (H), P.e.- infected control midguts (I), midguts expressing licorne RNAi in progenitors (J) and P.e.- infected midguts expressing licorne RNAi in progenitors (K)(progenitors from B). DNA is in blue. Scale bars are 20μm.

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Infection, Expressing, Control, MANN-WHITNEY, Activation Assay, Fluorescence

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: PGRP-LC is required in progenitors for ISC proliferation after P.e. infection (A). Depleting PGRP-LC by expressing PGRP-LC RNAi (1) in progenitors for 5 days with esg ts suppresses ISC proliferation by 80.4% compared to control P.e. -infected midguts (Mann–Whitney; p < 0.0001) (A). The mean number of PH3-positive cells per midgut with mean and 95% CI are shown for control midguts (n = 19 from one of two experiments), P.e. -infected control midguts (n = 19 from one of two experiments), midguts expressing PGRP-LC RNAi (1) in progenitor cells for 4 days (n = 20 from one of two experiments) and P.e.- infected midguts expressing PGRP-LC RNAi (1) in progenitors for 4 days (n = 17 from one of two experiments) (A). In A, the mean number of mitoses per midgut increased in P.e.- infected control midguts compared to uninfected control midguts (Mann-Whitney; p<0.0001). PGRP-LC is required in progenitors for p38 activation in progenitors and throughout the midgut epithelium after P.e. infection (B-K) . p38 activation is blocked in progenitors and throughout the midgut epithelium of P.e. -infected midguts expressing PGRP-LC RNAi (1) in progenitors by 81.7% (Mann-Whitney; p-value = 0.0079) and 71.5% (Mann-Whitney ; p-value = 0.0159), respectively, compared to control P.e. -infected midguts (B-C). In B, the mean p-p38 fluorescent intensity in progenitors per midgut with mean and 95% CI are shown for control midguts (n = 5 from one of two experiments), P.e. -infected control midguts (n = 5 from one of two experiments), midguts expressing PGRP-LC RNAi (1) in progenitors for 5 days (n = 5 from one of two experiments) and P.e. -infected midguts expressing PGRP-LC RNAi (1) in progenitors for 5 days (n = 5 from one of two experiments). In C, the epithelial p-p38 fluorescence intensity per midgut (from those analysed in B) are shown with mean and 95%CI. In B and C, the mean p-p38 fluorescence intensity increased in P.e.- infected control midguts compared to uninfected control midguts (Mann-Whitney; p value = 0.0556 in B; Mann-Whitney ; p-value = 0.0079 in C). p-p38 (D, E: red; D’, E’: LUT) increases in progenitors (E: GFP; E-E’: green-dashed outline) and throughout the midgut epithelium after P.e. infection compared to control (D-D’). Depleting PGRP-LC from progenitors for 5 days blocked the increase in p-p38 in progenitors and throughout the midgut epithelium (G-G’) compared to P.e .-infected control midguts (E-E’). The distribution (histogram) of p-p38 fluorescence intensity per progenitor is shown for uninfected control midguts (H), P.e.- infected control midguts (I), midguts expressing PGRP-LC RNAi (1) in progenitors (J) and P.e.- infected midguts expressing PGRP-LC RNAi (1) in progenitors (K) (progenitors from B). DNA is in blue. Scale bars are 20μm.

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Infection, Expressing, Control, MANN-WHITNEY, Activation Assay, Fluorescence

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: PGRP-LE is required in progenitors for ISC proliferation after P.e. infection (A). Depleting PGRP-LE by expressing PGRP-LE RNAi (1) in progenitors for 5 days with esg ts suppresses ISC proliferation by 107.0% compared to control P.e. -infected midguts (Mann–Whitney; p < 0.0001) (A). The mean number of PH3-positive cells per midgut with mean and 95% CI are shown for control midguts (n = 20 from one of two experiments), P.e. -infected control midguts (n = 24 from one of two experiments), midguts expressing PGRP-LE RNAi (1) in progenitor cells for 5 days (n = 28 from one of two experiments) and P.e.- infected midguts expressing PGRP-LC RNAi (1) in progenitors for 5 days (n = 25 from one of two experiments) (A). In A, the mean number of mitoses per midgut increased in P.e.- infected control midguts compared to uninfected control midguts (Mann-Whitney; p<0.0001). PGRP-LE is required in progenitors for p38 activation in progenitors and throughout the midgut epithelium after P.e. infection (B-K) . p38 activation is blocked in progenitors and throughout the midgut epithelium of P.e. -infected midguts expressing PGRP-LE RNAi (1) in progenitors by 63.1% (Mann–Whitney; p-value = 0.0317) and 61.7% (Mann–Whitney; p-value = 0.0317), respectively, compared to control P.e. -infected midguts (B-C). In B, the mean p-p38 fluorescent intensity in progenitors per midgut with mean and 95% CI are shown for control midguts (n = 5 from one of two experiments), P.e. -infected control midguts (n = 5 from one of two experiments), midguts expressing PGRP-LE RNAi (1) in progenitors for 5 days (n = 5 from one of two experiments) and P.e. -infected midguts expressing PGRP-LE RNAi (1) in progenitors for 5 days (n = 5 from one of two experiments). In C, the epithelial p-p38 fluorescence intensity per midgut (from those analysed in B) are shown with mean and 95%CI. In B and C, the mean p-p38 fluorescence intensity increased in P.e.- infected control midguts compared to uninfected control midguts (Mann–Whitney; p value = 0.0079 in B; Mann–Whitney; p-value = 0.0079 in C). p-p38 (D, E: red; D’, E’: LUT) increases in progenitors (E: GFP; E-E’: green-dashed outline) and throughout the midgut epithelium after P.e. infection compared to control (D-D’). Depleting PGRP-LE from progenitors for 5 days blocks the increase in p-p38 in progenitors and throughout the midgut epithelium (G-G’) compared to P.e .-infected control midguts (E-E’). The distribution (histogram) of p-p38 fluorescence intensity per progenitor is shown for uninfected control midguts (H), P.e.- infected control midguts (I), midguts expressing PGRP-LE RNAi (1) in progenitors (J) and P.e.- infected midguts expressing PGRP-LE RNAi (1) in progenitors (K)(progenitors from B). DNA is in blue. Scale bars are 20μm.

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Infection, Expressing, Control, MANN-WHITNEY, Activation Assay, Fluorescence

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: ISC proliferation is not required for p38 activation in progenitors and throughout the midgut epithelium after P.e. infection (A-C). Depleting the cdc25-homologue string by expressing string RNAi in progenitors for 2 days with esg ts suppresses ISC proliferation by 99.4% compared to control P.e. -infected midguts (Mann–Whitney; p < 0.0001) (A). The mean number of PH3-positive cells per midgut with mean and 95% CI are shown for control midguts (n = 22 from one experiment), P.e. -infected control midguts (n = 22 from one experiment), midguts expressing string RNAi (1) in progenitors for 2 days (n = 25 from one experiment) and P.e.- infected midguts expressing string RNAi (1) in progenitors for 2 days (n = 23 from one experiment) (A). In A, the mean number of mitoses per midgut increased in P.e.- infected control midguts compared to uninfected control midguts (Mann-Whitney; p<0.0001). ISC proliferation is not required for p38 activation in progenitors and throughout the midgut epithelium after P.e. infection (B-K) . p38 is activated in progenitors (Mann– Whitney; p-value = 0.0556) and throughout the midgut epithelium (Mann–Whitney; p-value = 0.0317) in P.e. -infected midguts expressing string RNAi in progenitors compared to control P.e. -infected midguts (B-C). In B, the mean p-p38 fluorescent intensity in progenitors per midgut with mean and 95% CI are shown for control midguts (n = 5 from one of two experiments), P.e. -infected control midguts (n = 5 from one of two experiments), midguts expressing string RNAi (1) in progenitors for 2 days (n = 5 from one of two experiments) and P.e. -infected midguts expressing string RNAi (1) in progenitors for 2 days (n = 5 from one of two experiments). In C, the epithelial p-p38 fluorescence intensity per midgut (from those analysed in B) are shown with mean and 95%CI. In B and C, the mean p-p38 fluorescence intensity increased in P.e.- infected control midguts compared to uninfected control midguts (Mann–Whitney; p value = 0.0317 in B; Mann–Whitney; p-value = 0.0079 in C). p-p38 (D, E: red; D’, E’: LUT) increases in progenitors (E: GFP; E-E’: green-dashed outline) and throughout the midgut epithelium after P.e. infection compared to control (D-D’). p38 is activated in progenitors and throughout the midgut epithelium after P.e. infection despite blocking ISC proliferation by depleting string from progenitors for 2 days (G-G’). The distribution (histogram) of p-p38 fluorescence intensity per progenitor is shown for uninfected control midguts (H), P.e.- infected control midguts (I), midguts expressing string RNAi in progenitors (J) and P.e.- infected midguts expressing string RNAi in progenitors (K) (progenitors from B). DNA is in blue. Scale bars are 20μm.

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Activation Assay, Infection, Expressing, Control, MANN-WHITNEY, Fluorescence, Blocking Assay

Journal: bioRxiv

Article Title: Recognition of pathogenic bacteria by intestinal progenitors promotes adult Drosophila midgut regeneration via PGRP-MKK3-p38 signalling

doi: 10.1101/2025.05.22.655543

Figure Lengend Snippet: Under homeostasis, pathogenic bacteria are not recognised by adult Drosophila midgut progenitors (ISCs and EBs) and the levels of activated p-p38 remain low within progenitors and throughout the midgut epithelium (A, A’) . After infection, bacterial peptidoglycan is recognised by both ISCs and EBs, inducing MKK3-p38 signalling. In ISCs, MKK3-p38 signalling promotes ISC proliferation; in both ISCs and EBs, MKK3-p38 signalling stimulates p38 activation throughout the epithelial regenerative niche (B, B’) .

Article Snippet: The following primary antibodies were used: rabbit polyclonal anti-phospho Ser 10 histone 3 (Millipore; 06-570; 1:1000), mouse monoclonal anti-phospho Ser 10 histone 3 (Sigma-Aldrich; 3H10; 05-806; 1:1000), rabbit monoclonal anti-phospho p38 (Thr180/Tyr182) (3D7)(Cell Signaling; 9215; 1:50) and rabbit polyclonal anti-phosphorylated p38 (Thr180/Tyr182) (Cell Signaling; 9211; 1:200).

Techniques: Bacteria, Infection, Activation Assay

Journal: Cell reports

Article Title: Restraint of inflammasome-driven cytokine responses through the mRNA stability protein TTP

doi: 10.1016/j.celrep.2025.115340

Figure Lengend Snippet:

Article Snippet: Rabbit polyclonal anti-phospho-p38 (Thr180/Tyr182) , Cell Signaling Technology , Cat# 9211; RRID:AB_331641.

Techniques: Recombinant, CyQUANT Assay, LDH Cytotoxicity Assay, Enzyme-linked Immunosorbent Assay, Software

Journal: Cell reports

Article Title: Non-cell-autonomous regulation of mTORC2 by Hedgehog signaling maintains lipid homeostasis

doi: 10.1016/j.celrep.2024.115191

Figure Lengend Snippet: (A) The rict-1/grd co-regulated genes are enriched for pmk-1 -dependent genes (hypergeometric p value reported ). (B) Quantification of lipid levels using Nile Red staining (day 1 adults reared at 20°C; mean ± SD; ** p < 0.01; *** p < 0.001; **** p < 0.0001; one-way ANOVA). (C) A heatmap showing differential expression values (log2 fold change relative to WT) of the 1,632 grd -dependent genes ( R 2 values are shown for the indicated comparisons). (D–G) Western blot and quantification of phospho-p38/PMK-1 levels for (D and E) C. elegans lysates prepared from WT, rict-1(mg360) , grd , or nsy-1(ums8) mutants ( ums8 is a gain-of-function allele; mean ± SEM; * p < 0.05; n.s., not significant; one-way ANOVA) and (F and G) AML12 hepatocytes treated with SAG for increasing amounts of time (10- or 15-min time point quantified; mean ± SEM; ** p < 0.01; t test). (H) A model of how Hh governs intestinal metabolism through the dual regulation of mTORC2 and p38 signaling in C. elegans . See also .

Article Snippet: Rabbit polyclonal anti-phospho-p38 MAPK (Thr180/Tyr182) , Cell Signaling Technology , Cat# 9211; RRID:AB_331641.

Techniques: Staining, Quantitative Proteomics, Western Blot

Journal: Cell reports

Article Title: Non-cell-autonomous regulation of mTORC2 by Hedgehog signaling maintains lipid homeostasis

doi: 10.1016/j.celrep.2024.115191

Figure Lengend Snippet: key resources table

Article Snippet: Rabbit polyclonal anti-phospho-p38 MAPK (Thr180/Tyr182) , Cell Signaling Technology , Cat# 9211; RRID:AB_331641.

Techniques: Virus, Recombinant, SYBR Green Assay, Transfection, DC Protein Assay, Mutagenesis, CRISPR, Plasmid Preparation, Software

Journal: PLOS ONE

Article Title: The CXCR4 antagonist R54 targets epithelial-mesenchymal transition (EMT) in human ovarian cancer cells

doi: 10.1371/journal.pone.0314735

Figure Lengend Snippet: Western blot for p-ERK, p-AKT, p-p38 and RAC1 protein levels after 10 minutes of stimulation with CXCL12 100 ng/mL ± R54 100 nM.

Article Snippet: Blots were incubated with 1:1000 mouse anti-CXCR4 antibody (cat n. 60042-1-Ig Proteintech), 1:1000 rabbit polyclonal anti-phospho-p44/42 MAPK (ERK1/2) (Thr202/Tyr204) antibody (cat n. 9101 Cell Signaling Technology), 1:1000 rabbit polyclonal anti-p44/42 MAPK (ERK1/2) antibody (cat n. 9102 Cell Signaling Technology), 1:1000 rabbit polyclonal anti-phospho-AKT (Ser 473) antibody (cat n. 9271 Cell Signaling Technology), 1:1000 rabbit polyclonal anti-AKT antibody (cat n. 9272 Cell Signaling Technology), 1:1000 rabbit polyclonal anti-phospho-p38 MAPK (Thr180/Tyr182) (D3F9) XP antibody (cat n. 4511 Cell Signaling Technology), 1:1000 rabbit polyclonal anti-p38 MAPK antibody (cat n. 9212 Cell Signaling Technology), 1:1000 mouse monoclonal anti-RAC 1/2/3 Antibody G-2 (cat n. sc-514583 200 μg/ml Santa Cruz Biotechnology, INC.), 1:1000 anti-E-CADHERIN (24E10) rabbit mAb (cat n. 3195 Cell Signaling Technology), 1:1000 anti-VIMENTIN (D21H3) XP rabbit mAb (cat n. 5741 Cell Signaling Technology), 1:1000 anti-BETA-CATENIN (D10A8) XP rabbit mAb (cat n. 480 Cell Signaling Technology), 1:20000 monoclonal mouse anti–α-tubulin antibody (cat n. T9026 Sigma-Aldrich) in TBS containing 5% BSA and 0,01% Sodium Azide overnight at 4°C.

Techniques: Western Blot