Journal: medRxiv

Article Title: Polymorphism in IFNAR contributes to glucocorticoid response and outcome in ARDS and COVID-19

doi: 10.1101/2022.03.10.22272123

Figure Lengend Snippet: (A ) STAT1 expression in the lung after 4-day culture in the presence of IFN beta with or without hydrocortisone (HC). ( B) pSTAT1 expression in the same specimens as in A. ( C) Example photomicrographs showing higher STAT2 expression in a TT patient than in a CT patient and the effect of HC on its nuclear translocation. Most STAT2 remains in the cytoplasm of the CT patients, whereas nuclear expression is prominent in the TT patient. Indicated insets are shown in the bottom row. Arrows. ( D ) Combined results of all patients noting that two CT samples are excluded in the data as the patients were already under glucocorticoid treatment at the time of sample acquisition. Ns, not significant; *P<0.05; **P<0.01; and ***P<0.001

Article Snippet: The first stage antibodies were anti-alpha chain of the IFN alpha/beta receptor (St John’s Laboratory STJ112765) that was used 1:2000 and 1:5000 and anti-Stat1 (1:400, 9175S), anti-pStat1(1:100, 9167S) and anti-Stat2 (1:200, 72604S) all from Cell Signalling.

Techniques: Expressing, Translocation Assay

Journal: Brain, behavior, and immunity

Article Title: Alcohol Exposure after Mild Focal Traumatic Brain Injury Impairs Neurological Recovery and Exacerbates Localized Neuroinflammation

doi: 10.1016/j.bbi.2014.11.006

Figure Lengend Snippet: Diagram of coronal rat brain section showing the site of injury and photographed region (4 A). Representative immunofluorescence images (10 ×) of ipsilateral cortex GFAP, ED-1, and HMGB1 immunoreactivity (green) combined with DAPI (blue) at 14 days post-TBI (10 days post-alcohol exposure) (4 B).

Article Snippet: Anti-HMGB1 Rabbit polyclonal (Abcam, Cambridge, UK) , 1:100 , Donkey anti-Rabbit Alexa Fluor 488 (Invitrogen, Carlsbad, CA) , 1:200.

Techniques: Immunofluorescence

Journal: Brain, behavior, and immunity

Article Title: Alcohol Exposure after Mild Focal Traumatic Brain Injury Impairs Neurological Recovery and Exacerbates Localized Neuroinflammation

doi: 10.1016/j.bbi.2014.11.006

Figure Lengend Snippet: Quantification of ipsilateral cortex GFAP, ED-1, and HMGB1 immunoreactivity at 14 days post-TBI (10 days post-alcohol exposure). Images are quantified as % area of positive staining in 1.035 mm2 (10×). Values are shown as means ± SEM. For GFAP and ED-1, Sham/Air n = 4, Sham/Alcohol n = 4, TBI/Air n = 4, TBI/Alcohol n = 6. For HMGB1, Sham/Air n = 4, Sham/Alcohol n = 5, TBI/Air n = 5, TBI/Alcohol n = 7 (each n represents the average of 3 images taken from each animal) * p < 0.05 of the TBI groups vs. time-matched sham controls; $ p < 0.05 of the TBI/Alcohol group vs. TBI/Air group, by two-way ANOVA (5 A, 5 C, and 5 E).

Article Snippet: Anti-HMGB1 Rabbit polyclonal (Abcam, Cambridge, UK) , 1:100 , Donkey anti-Rabbit Alexa Fluor 488 (Invitrogen, Carlsbad, CA) , 1:200.

Techniques: Staining

Journal: Brain, behavior, and immunity

Article Title: Alcohol Exposure after Mild Focal Traumatic Brain Injury Impairs Neurological Recovery and Exacerbates Localized Neuroinflammation

doi: 10.1016/j.bbi.2014.11.006

Figure Lengend Snippet: Primary and Secondary Antibodies.

Article Snippet: Anti-HMGB1 Rabbit polyclonal (Abcam, Cambridge, UK) , 1:100 , Donkey anti-Rabbit Alexa Fluor 488 (Invitrogen, Carlsbad, CA) , 1:200.

Techniques: Concentration Assay

Journal: Poultry Science

Article Title: Characterization and functional analyses of novel chicken leukocyte immunoglobulin-like receptor subfamily B members 4 and 5

doi: 10.3382/ps/pez442

Figure Lengend Snippet: LILRB4R, -B4S, -B5R, and -B5S glycoprotein regulated the JAK-STAT signaling pathway. ( A ) Western blotting results of JAK2/TYK2, STAT1/3, and SOCS1 after LILRB4–5 transfection of HD11 cell line. ( B ) Changes in mRNA levels of JAK2/TYK2, STAT1/3 and SOCS1 genes after LILRB4–5 transfection in HD11 cell line were detected by qRT-PCR. Data are presented as the mean ± SEM ( n = 3) of 3 independent experiments: * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: The following reagents were from the indicated manufacturers: mouse anti-chicken MHC Class I-PE and mouse anti-chicken β2m-PE antibody (Southern Biotech, Birmingham, AL, USA); rabbit anti-chicken STAT1 (phospho-Ser 727 ), anti-chicken STAT3 (phospho-Ser 727 ), and anti-chicken JAK2 (phospho-Tyr 1007 /Tyr 1008 ) antibody (Santa Cruz Biotech Dallas, Texas, USA); rabbit anti-chicken SOCS1, anti-chicken STAT1, anti-chicken STAT3 antibodies, horseradish peroxidase ( HRP )-linked anti-rabbit secondary antibodies, and protein G–sepharose bead (Sigma-Aldrich, Louis, MO, USA); rabbit anti-chicken SHP2 (phospho-Tyr 542 ), anti-chicken JAK2, and anti-chicken TYK2 antibody (Biorbyt, San Francisco, CA, USA); rabbit anti-chicken GAPDH antibody (Abcam, Cambridge, MA, USA); Alexa Fluor® 488 Goat anti-rabbit IgG (H+L) secondary antibody (Invitrogen, Carlsbad, CA, USA); mouse monoclonal anti-chicken IFN-γ, IL-17A, IL-12p40 antibody and recombinants of these proteins (kindly provided by Dr. Hyun S. Lillehoj, USDA).

Techniques: Western Blot, Transfection, Quantitative RT-PCR

Journal: JNCI Journal of the National Cancer Institute

Article Title: Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1–BCR-ABL–JAK2 Complex

doi: 10.1093/jnci/djt006

Figure Lengend Snippet: Evidence of Abelson helper integration site 1 (Ahi-1)–Janus kinase 2 (Jak2) and Ahi-1-BCR-ABL interactions in BCR-ABL – and Jak2 -transduced cells coexpressing Ahi-1 and its mutants. A) Schematic of functional domains of full-length and mutant (N-ter∆) Ahi-1. Vectors were transduced into BaF3 cells and BCR-ABL –inducible cells, and increased protein expression levels of full-length and mutant Ahi-1 were detected by Western blotting. B) Ahi-1 ( left panel ) or Jak2 ( right panel ) were immunoprecipitated from lysates of the same transduced cells and then electrophoresed and probed with specific antibodies, as indicated. C) Human influenza hemagglutinin (HA)–tagged SH3 ∆ or SH3WD40 ∆ mutants were transfected into 293T cells with or without a Jak2 vector, immunoprecipitated with antibodies to either HA or Jak2, electrophoresed, and probed using Jak2 or Ahi-1 antibodies ( left panel ). The right panel shows that these two mutants were coexpressed with BCR-ABL , immunoprecipitated with an anti-HA antibody, and probed with a c-ABL antibody. A schematic of the functional domains of full-length Ahi-1 and its SH3 ∆ and SH3WD40 ∆ mutants is below the right panel. IP = immunoprecipitation; WB = Western blotting.

Article Snippet: The antibodies in this study included a rabbit polyclonal N-terminal AHI-1 antibody and an antimouse Ahi-1 mouse monoclonal antibody (1:1000 dilution) (C-mAhi-1 M5, Applied Biological Materials Inc Vancouver, BC, Canada), an antimouse ABL mouse monoclonal antibody (1:1000 dilution) (8E9; BD Biosciences), an antimouse JAK2 rabbit monoclonal antibody (1:1000 dilution) (Cell signaling Technology, MA), a rabbit polyclonal anti-JAK2 agarose conjugated antibody (Santa Cruz Biotechnology), anti-phospho-JAK2 rabbit polyclonal antibodies (1:1000 dilution) (Cell Signaling and Epitomics Inc, Burlingame, CA), an antihuman STAT5 rabbit polyclonal antibody (1:1000 dilution) (Millipore, Billeria, MA), an anti-phospho-STAT5 rabbit monoclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-CRKL rabbit polyclonal antibody (1:2000 dilution) (Cell Signaling), an antihuman CRKL rabbit polyclonal antibody (1:1000 dilution) (Santa Cruz Biotechonolgy), an antiphosphotyrosine mouse monoclonal antibody (4G10) (1:2000 dilution) (Millipore, Billerica, MA), an anti-phospho-AKT rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antimouse Akt rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-ERK rabbit polyclonal antibody (1:1000 dilution), an antirat ERK rabbit polyclonal (1:1000 dilution), an antimouse GAPDH mouse monoclonal antibody (1:2000 dilution) (Sigma Aldrich), an antiactin mouse monoclonal antibody (1:1000 dilution) (Sigma Aldrich), and an anti-HA mouse monoclonal antibody (1:1000 dilution) (Applied Biological Materials Inc).

Techniques: Functional Assay, Mutagenesis, Expressing, Western Blot, Immunoprecipitation, Transfection, Plasmid Preparation

Journal: JNCI Journal of the National Cancer Institute

Article Title: Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1–BCR-ABL–JAK2 Complex

doi: 10.1093/jnci/djt006

Figure Lengend Snippet: Effect of imatinib (IM) on induction of apoptosis and inhibition of colony formation in BCR-ABL –transduced cells coexpressing Abelson helper integration site 1 ( Ahi-1 ) mutants and combined treatment with IM and a Janus kinase 2 (JAK2) inhibitor on inhibition of growth of AHI-1 –overexpressing and IM-resistant cells. A) BCR-ABL –transduced cells coexpressing full-length Ahi-1 and its mutants were cultured with IM, and the treated cells were stained with Annexin V/7-aminoactinomysin (7-AAD) to detect apoptotic cells after 24 or 48 hours. Representative fluorescence-activated cell sorting plots showing detection of Annexin V/7-AAD + cells 24 hours after IM treatment are included. B) Transduced cells (200 cells/group) were pretreated with IM for 24 hours and then plated in colony-forming cell assays. Colony numbers produced in semisolid media were counted and expressed as a percentage of counts obtained from control cells without any drug added. C–E) Control K562 cells, AHI-1 –transduced SH4-bulk K562 cells (with suppressed AHI-1 expression), lenti-AHI-1 K652 cells (overexpressing AHI-1 ) and IM-resistant K562 cells were incubated with IM ( C ), or TG101209 (TG) alone ( D ), or both in combination ( E ), or with no drug for 48 hours and the percentage of viable cells was then measured. F) AHI-1 was immunoprecipitated from cell lysates of AHI-1 –overexpressing K562 cells treated with IM and TG alone or in combination for 16 hours. The immunoprecipitates were then probed with an antityrosine phosphorylation antibody (4G10), a BCR-ABL antibody, a JAK2 antibody, and an AHI-1 antibody. Control cells = Hut78 cells. Data are means, and error bars represent 95% confidence intervals from three independent experiments in triplicate. P values were calculated using a two-sided Student t test. WB = Western blotting.

Article Snippet: The antibodies in this study included a rabbit polyclonal N-terminal AHI-1 antibody and an antimouse Ahi-1 mouse monoclonal antibody (1:1000 dilution) (C-mAhi-1 M5, Applied Biological Materials Inc Vancouver, BC, Canada), an antimouse ABL mouse monoclonal antibody (1:1000 dilution) (8E9; BD Biosciences), an antimouse JAK2 rabbit monoclonal antibody (1:1000 dilution) (Cell signaling Technology, MA), a rabbit polyclonal anti-JAK2 agarose conjugated antibody (Santa Cruz Biotechnology), anti-phospho-JAK2 rabbit polyclonal antibodies (1:1000 dilution) (Cell Signaling and Epitomics Inc, Burlingame, CA), an antihuman STAT5 rabbit polyclonal antibody (1:1000 dilution) (Millipore, Billeria, MA), an anti-phospho-STAT5 rabbit monoclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-CRKL rabbit polyclonal antibody (1:2000 dilution) (Cell Signaling), an antihuman CRKL rabbit polyclonal antibody (1:1000 dilution) (Santa Cruz Biotechonolgy), an antiphosphotyrosine mouse monoclonal antibody (4G10) (1:2000 dilution) (Millipore, Billerica, MA), an anti-phospho-AKT rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antimouse Akt rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-ERK rabbit polyclonal antibody (1:1000 dilution), an antirat ERK rabbit polyclonal (1:1000 dilution), an antimouse GAPDH mouse monoclonal antibody (1:2000 dilution) (Sigma Aldrich), an antiactin mouse monoclonal antibody (1:1000 dilution) (Sigma Aldrich), and an anti-HA mouse monoclonal antibody (1:1000 dilution) (Applied Biological Materials Inc).

Techniques: Inhibition, Cell Culture, Staining, Fluorescence, FACS, Produced, Control, Expressing, Incubation, Immunoprecipitation, Phospho-proteomics, Western Blot

Journal: JNCI Journal of the National Cancer Institute

Article Title: Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1–BCR-ABL–JAK2 Complex

doi: 10.1093/jnci/djt006

Figure Lengend Snippet: Inhibition of phosphorylation of BCR-ABL, CRK-like (CRKL), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 5 (STAT5) in transduced K562 cells in response to combined treatment with TG101209 (TG) and imatinib (IM). A) K562 cells, Abelson helper integration site 1 ( AHI-1 )–overexpressing K562 cells, and IM-resistant K562 cells (IMR) were cultured with or without IM, TG, or a combination of IM and TG for 16 hours. Western blot analysis detected phosphorylation and protein expression of various proteins using the specific antibodies indicated. B) BV173 cells were treated with IM, TG, or IM plus TG for 16 hours. Cell lysates were immuno-probed with the specific antibodies indicated. GAPDH or actin was utilized as a loading control.

Article Snippet: The antibodies in this study included a rabbit polyclonal N-terminal AHI-1 antibody and an antimouse Ahi-1 mouse monoclonal antibody (1:1000 dilution) (C-mAhi-1 M5, Applied Biological Materials Inc Vancouver, BC, Canada), an antimouse ABL mouse monoclonal antibody (1:1000 dilution) (8E9; BD Biosciences), an antimouse JAK2 rabbit monoclonal antibody (1:1000 dilution) (Cell signaling Technology, MA), a rabbit polyclonal anti-JAK2 agarose conjugated antibody (Santa Cruz Biotechnology), anti-phospho-JAK2 rabbit polyclonal antibodies (1:1000 dilution) (Cell Signaling and Epitomics Inc, Burlingame, CA), an antihuman STAT5 rabbit polyclonal antibody (1:1000 dilution) (Millipore, Billeria, MA), an anti-phospho-STAT5 rabbit monoclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-CRKL rabbit polyclonal antibody (1:2000 dilution) (Cell Signaling), an antihuman CRKL rabbit polyclonal antibody (1:1000 dilution) (Santa Cruz Biotechonolgy), an antiphosphotyrosine mouse monoclonal antibody (4G10) (1:2000 dilution) (Millipore, Billerica, MA), an anti-phospho-AKT rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antimouse Akt rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-ERK rabbit polyclonal antibody (1:1000 dilution), an antirat ERK rabbit polyclonal (1:1000 dilution), an antimouse GAPDH mouse monoclonal antibody (1:2000 dilution) (Sigma Aldrich), an antiactin mouse monoclonal antibody (1:1000 dilution) (Sigma Aldrich), and an anti-HA mouse monoclonal antibody (1:1000 dilution) (Applied Biological Materials Inc).

Techniques: Inhibition, Phospho-proteomics, Cell Culture, Western Blot, Expressing, Control

Journal: JNCI Journal of the National Cancer Institute

Article Title: Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1–BCR-ABL–JAK2 Complex

doi: 10.1093/jnci/djt006

Figure Lengend Snippet: Effects of oral administration of TG101209 (TG) and imatinib (IM) on elimination of chronic myeloid leukemia (CML) BV173 cells and survival of leukemic mice in immunodeficient mice. A) BV173 cells were cultured with 1.0 µM IM, 0.5 µM TG, IM plus TG, or no drug for 3 days, and the progeny recovered from 2.5×10 6 initial cells were then injected intravenously into NOD/SCID–interleukin 2 receptor γ–chain-deficient (NSG) mice (n = 6 mice per condition). The left panel shows fluorescence-activated cell sorting profiles of engrafted human CD19/20 + cells detected in bone marrow aspirates of representative mice obtained 3 weeks posttransplant. The percentage of human CD19/20 + BV173 cells detected in the bone marrow of mice examined 3 weeks after injection is shown in the right panel . Data are means, and error bars represent 95% confidence intervals of six measurements per condition. B) Survival curve for recipients of BV173 cells (2.5×10 6 per mouse; n = 6 mice per group) treated by oral gavage beginning at 2 weeks posttransplant with vehicle, IM (50mg/kg), TG (60mg/kg), and IM (50mg/kg) plus TG (60mg/kg) twice a day for 2 weeks. Statistically significantly prolonged survival was observed in mice receiving the combination treatment ( left panel ). Body weights of mice in each treated group were measured, as indicated in the right panel . Log-rank tests were used to compare median survival of different groups (n = 6 mice per group), and P values were calculated using a two-sided Student t test. C) Model of the mechanism by which Abelson helper integration site 1 (AHI-1)–BCR-ABL and AHI-1–Janus kinase 2 (JAK2) interactions regulate constitutive activation of BCR-ABL and JAK2/ signal transducer and activator of transcription 5 (STAT5), resulting in increased leukemic stem cell proliferation, survival and maintenance and reduced tyrosine kinase inhibitor (TKI) response of these cells. Targeting both BCR-ABL and JAK2 activities to destabilize this complex perturbs these biological properties. IL-3 = interleukin 3; IL-3R = interleukin 3 receptor.

Article Snippet: The antibodies in this study included a rabbit polyclonal N-terminal AHI-1 antibody and an antimouse Ahi-1 mouse monoclonal antibody (1:1000 dilution) (C-mAhi-1 M5, Applied Biological Materials Inc Vancouver, BC, Canada), an antimouse ABL mouse monoclonal antibody (1:1000 dilution) (8E9; BD Biosciences), an antimouse JAK2 rabbit monoclonal antibody (1:1000 dilution) (Cell signaling Technology, MA), a rabbit polyclonal anti-JAK2 agarose conjugated antibody (Santa Cruz Biotechnology), anti-phospho-JAK2 rabbit polyclonal antibodies (1:1000 dilution) (Cell Signaling and Epitomics Inc, Burlingame, CA), an antihuman STAT5 rabbit polyclonal antibody (1:1000 dilution) (Millipore, Billeria, MA), an anti-phospho-STAT5 rabbit monoclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-CRKL rabbit polyclonal antibody (1:2000 dilution) (Cell Signaling), an antihuman CRKL rabbit polyclonal antibody (1:1000 dilution) (Santa Cruz Biotechonolgy), an antiphosphotyrosine mouse monoclonal antibody (4G10) (1:2000 dilution) (Millipore, Billerica, MA), an anti-phospho-AKT rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antimouse Akt rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling), an antihuman phospho-ERK rabbit polyclonal antibody (1:1000 dilution), an antirat ERK rabbit polyclonal (1:1000 dilution), an antimouse GAPDH mouse monoclonal antibody (1:2000 dilution) (Sigma Aldrich), an antiactin mouse monoclonal antibody (1:1000 dilution) (Sigma Aldrich), and an anti-HA mouse monoclonal antibody (1:1000 dilution) (Applied Biological Materials Inc).

Techniques: Cell Culture, Injection, Fluorescence, FACS, Activation Assay

Journal: Scientific Reports

Article Title: LncTUG1 promotes hepatocellular carcinoma immune evasion via upregulating PD-L1 expression

doi: 10.1038/s41598-023-42948-8

Figure Lengend Snippet: TUG1 affects the JAK2/ STAT3 pathway to regulate PD-L1. ( A ): The relative mRNA expression of JAK2 was analyzed in shTUG1 HCC cells. ( B ): The relative mRNA expression of STAT3 was analyzed in shTUG1 HCC cells. ( C ): The protein levels of pJAK2, JAK2, pSTAT3, STAT3, PD-L1 were analyzed in shTUG1 HCC cells by western blotting. ( D ) pJAK2, JAK2,and PDL1 protein levels are assessed by immunoblotting in HCC-LM3 cell was transfected with TUG1 silenced (shTUG1) and/or JAK2 overexpressed (JAK2-OE). ( E ) pSTAT3,STAT3,and PDL1 protein levels are assessed by immunoblotting in HCC-LM3 cell was transfected with TUG1 silenced (shTUG1) and/or STAT3 overexpressed (STAT3-OE).

Article Snippet: Protein detection was performed by using the following primary antibodies: anti-PD-L1 (ab205921, Abcam), anti-GAPDH (ab8245, Abcam), anti-JAK2 (#3230, Cell Signaling Technology), anti-pJAK2 Tyr1007/1008 (#3771,Cell Signaling Technology),anti-STAT3 (#9139, Cell Signaling Technology), anti-pSTAT3 Tyr705 (#9145, Cell Signaling Technology).

Techniques: Expressing, Western Blot, Transfection

Journal: Oncology reports

Article Title: Silibinin downregulates MMP2 expression via Jak2/STAT3 pathway and inhibits the migration and invasive potential in MDA-MB-231 cells.

doi: 10.3892/or.2017.5588

Figure Lengend Snippet: Figure 2. Silibinin downregulates the expression of Jak2/STAT3 signaling proteins in a dose- and time-dependent manner. (A) Western blot analyses showing the concentration dependent effect of silibinin in MDA‑MB‑231 cells following exposure to silibinin for 24 h. (B) Relative levels of the pSTAT3, STAT3, pJak2, and Jak2 proteins. (C) Time-dependent effect of silibinin on protein expression in MDA‑MB‑231 cells. (D) Relative expression levels of pSTAT3, STAT3, pJak2, and Jak2, measured using densitometry. These data were normalized to actin levels, and then shown as a percentage of the control. The data presented are representative of three independent experiments. Statistical analyses were conducted using the t-test (**p<0.01, ***p<0.001).

Article Snippet: An anti phosphor Jak2 antibody (Tyrosine residue 1007/1008) was purchased from Cell Signaling Technology (Beverly, MA, USA).

Techniques: Expressing, Western Blot, Concentration Assay, Control

Journal: Oncology reports

Article Title: Silibinin downregulates MMP2 expression via Jak2/STAT3 pathway and inhibits the migration and invasive potential in MDA-MB-231 cells.

doi: 10.3892/or.2017.5588

Figure Lengend Snippet: Figure 7. Schematic representation of the inhibition of invasive mechanisms provoked by silibinin in MDA‑MB‑231 cells. Silibinin inhibits Jak2 expression and phosphorylation, resulting, in turn, in the inhibition of STAT3 expression, phosphorylation, nuclear translocation, and DNA binding activity. Consequently, STAT3's down-stream targets are inhibited (including MMP2), resulting in reduced cell migration and invasion.

Article Snippet: An anti phosphor Jak2 antibody (Tyrosine residue 1007/1008) was purchased from Cell Signaling Technology (Beverly, MA, USA).

Techniques: Inhibition, Expressing, Phospho-proteomics, Translocation Assay, Binding Assay, Activity Assay, Migration