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anti paxl y779  (R&D Systems)


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    R&D Systems anti paxl y779
    Anti Paxl Y779, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phospho+axl+y779/Human+Phospho-Axl+(Y779)+Antibody/pmc12595455__pnas%2E2502778122%2Esapp-2-25-27
    Average 93 stars, based on 55 article reviews
    anti paxl y779 - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: Targeting the Axl and mTOR Pathway Synergizes Immunotherapy and Chemotherapy to Butylidenephthalide in a Recurrent GBM
    Article Snippet: Protein lysates of primary culture cells isolated from the GBM were resolved on sodium dodecyl sulfate-polyacrylamide gels (SDS-PAGEs) and electro-transferred to polyvinylidene fluoride (PVDF) membrane (Merck Millipore) in a wet blot format. .. After protein transfer, the membranes were blocked with blocking buffer (5% non-fat dry milk powder, dissolved in 0.1% PBS-Tween 20) and incubated with primary antibodies against MGMT (2739S, Cell Signaling, Beverly, MA, USA), EGFR (GTX628887, GeneTex, Hsinchu, Taiwan), EGFR (phosphor Tyr1068) (GTX132810, GeneTex, Hsinchu, Taiwan), Axl (H-124) (sc-20741, Santa Cruz Biotechnology, Dallas, TX, USA), phospho-Axl (Y779) (MAB6965, R&D Systems, Minneapolis, MN, USA), mTOR (AB32028, Abcam), phospho-mTOR (Ser2448) (5536S, Cell Signaling), PD-L1 (14-5982-85, Thermo Fisher Scientific, Waltham, MA, USA), or β -actin (A5441, Sigma-Aldrich) that were diluted in blocking buffer and incubated overnight at 4°C. ..

    Incubation:

    Article Title: Targeting the Axl and mTOR Pathway Synergizes Immunotherapy and Chemotherapy to Butylidenephthalide in a Recurrent GBM
    Article Snippet: Protein lysates of primary culture cells isolated from the GBM were resolved on sodium dodecyl sulfate-polyacrylamide gels (SDS-PAGEs) and electro-transferred to polyvinylidene fluoride (PVDF) membrane (Merck Millipore) in a wet blot format. .. After protein transfer, the membranes were blocked with blocking buffer (5% non-fat dry milk powder, dissolved in 0.1% PBS-Tween 20) and incubated with primary antibodies against MGMT (2739S, Cell Signaling, Beverly, MA, USA), EGFR (GTX628887, GeneTex, Hsinchu, Taiwan), EGFR (phosphor Tyr1068) (GTX132810, GeneTex, Hsinchu, Taiwan), Axl (H-124) (sc-20741, Santa Cruz Biotechnology, Dallas, TX, USA), phospho-Axl (Y779) (MAB6965, R&D Systems, Minneapolis, MN, USA), mTOR (AB32028, Abcam), phospho-mTOR (Ser2448) (5536S, Cell Signaling), PD-L1 (14-5982-85, Thermo Fisher Scientific, Waltham, MA, USA), or β -actin (A5441, Sigma-Aldrich) that were diluted in blocking buffer and incubated overnight at 4°C. ..

    Western Blot:

    Article Title: Growth arrest-specific protein 6 deficiency impairs liver tissue repair after acute toxic hepatitis in mice.
    Article Snippet: Fluorescent labeling of CD68 was achieved using secondary FITC coupled anti-rat IgG STAR 80F (Serotec). .. Fifty lg of protein from snap frozen liver were used for Western blotting as previously described [16] using antibodies against PCNA (Sigma), phospho-Axl-Y779 (R & D systems), Axl (Santa Cruz) and phosphoNFkBp65-Ser536 (Cell Signaling). .. Anti-b-actin clone AC15 antibody (Sigma) was used to correct for unequal loadings.

    Article Title: Targeting Tyro3, Axl, and MerTK Receptor Tyrosine Kinases Significantly Sensitizes Triple-Negative Breast Cancer to CDK4/6 Inhibition
    Article Snippet: Proteins were separated using SDS-PAGE (Gel = Bolt 4–12% Bis-Tris, Invitrogen (Waltham, MA, USA), NW04120BOX), transferred onto the PVDF membranes (Immobilon-FL, Millipore Sigma, (St. Louis, MO, USA), IPFL00005), and subsequently blocked (Intercept Blocking Buffer, Li-Cor, Lincoln, NE, USA, 92760001) for 1 h prior to the addition of primary antibodies. .. The following antibodies were used for immunoblotting: phospho-Met (Tyr1234/1235) (CST, 3077), Met (D1C2) (CST, 8198), Axl (C89E7) (CST, 8661), phospho-Axl (Y779) (R&D Systems, MAB6965), phospho-MerTK (Phosphosolutions, Denver, CO, USA, p186-749), MerTK (Abcam, Cambridge, UK, ab52968), phospho-Akt (CST, 9271), phospho-mTOR (abclonal, AP0094), and ERBB2 (CST, 2165). .. Actin (A5441) and GAPDH (G9545) were from Sigma-Aldrich (St. Louis, MO, USA).

    Article Title: SKI‐G‐801, an AXL kinase inhibitor, blocks metastasis through inducing anti‐tumor immune responses and potentiates anti‐PD‐1 therapy in mouse cancer models
    Article Snippet: Equivalent amounts of protein were separated using the NuPAGE 4–12% Bis–Tris Gel System (Invitrogen) and then transferred to polyvinylidene difluoride membranes. .. Membranes were probed with anti‐phospho‐AXL (Y702) (1:1000, CTS, #5724; Cell Signaling Technology, MA, USA), anti‐phospho‐AXL (Y779) (1:1000; R&D, AF2228; R&D Systems, NE, USA), anti‐phospho‐FLT3 (Y842) (1:1000, CTS, #4577; Cell Signaling Technology), anti‐phospho‐H3 (S28) (1:1000, CTS, #9713; Cell Signaling Technology) or anti‐phospho‐KDR (Y1175) (1:1000, CTS, #2478; Cell Signaling Technology) antibodies and then stripped with Restore Western Blot Stripping Buffer (Thermo Scientific). .. The membranes were then probed again with anti‐AXL (1:1000, CTS, #8661; Cell Signaling Technology), anti‐H3 (1:1000, CTS, #3638; Cell Signaling Technology), anti‐FLT3 (1:1000, CTS, #3462; Cell Signaling Technology) or anti‐actin (1:1000, #MAB1501; Sigma‐Aldrich) antibodies.

    Article Title: Gilteritinib, a FLT3/AXL inhibitor, shows antileukemic activity in mouse models of FLT3 mutated acute myeloid leukemia
    Article Snippet: MV4–11-AXL cells, which exogenously express AXL, were also prepared at Astellas Pharma Inc. Ba/F3 cells expressing FLT3-ITD, FLT3-D835Y, FLT3-ITD-D835Y, FLT3-ITD-F691 L, or FLT3-ITD-F691I mutations (FLT3-ITD_Ba/F3, FLT3-D835Y_Ba/F3, FLT3-ITD-D835Y_Ba/F3, FLT3-ITD-F691L_Ba/F3, FLT3-ITD-F691I_Ba/F3) were established by Astellas Pharma Inc. .. The following antibodies were used for immunoblotting: FLT3 (Abcam, Cambridge, MA); phosphorylated pan-tyrosine (Merck Millipore, Billerica, MA); p44/42 MAPK (ERK1/2), phospho-p44/42 MAPK (ERK1/2) (Thr202/Tyr204) (197G2) (E10), AKT, phospho-AKT (Ser473) (193H12), and AXL (C44G1) (Cell Signaling Technology, Danvers, MA); STAT5 and phospho-STAT5 (Y694) (BD Biosciences, Franklin Lakes, NJ); phospho-AXL (Y779) (MAB6965, R&D Systems, Minneapolis, MN); and β-actin (Sigma-Aldrich, St. Louis, MO). .. The kinase inhibitory activity of gilteritinib was tested against a panel of 78 TKs (Table S1) using ATP concentrations that were approximately equal to the K m value for each kinase in a TK-ELISA or off-chip mobility shift assay (MSA) at Carna Biosciences, Inc. (Kobe, Japan).

    Affinity Purification:

    Article Title: Identification of Axl as a downstream effector of TGF-β1 during Langerhans cell differentiation and epidermal homeostasis
    Article Snippet: .. For the detection of phosphorylated Axl, an affinity-purified rabbit anti–phospho-Axl (Y779) Ab (1:100; R&D Systems) was used. .. Five male TAM KO mice and five age- and sex-matched WT control mice were shaved, and their abdomens were exposed to 0.5% DNFB (Sigma-Aldrich) in 4:1 acetone/olive oil (40 μl).

    Stripping:

    Article Title: SKI‐G‐801, an AXL kinase inhibitor, blocks metastasis through inducing anti‐tumor immune responses and potentiates anti‐PD‐1 therapy in mouse cancer models
    Article Snippet: Equivalent amounts of protein were separated using the NuPAGE 4–12% Bis–Tris Gel System (Invitrogen) and then transferred to polyvinylidene difluoride membranes. .. Membranes were probed with anti‐phospho‐AXL (Y702) (1:1000, CTS, #5724; Cell Signaling Technology, MA, USA), anti‐phospho‐AXL (Y779) (1:1000; R&D, AF2228; R&D Systems, NE, USA), anti‐phospho‐FLT3 (Y842) (1:1000, CTS, #4577; Cell Signaling Technology), anti‐phospho‐H3 (S28) (1:1000, CTS, #9713; Cell Signaling Technology) or anti‐phospho‐KDR (Y1175) (1:1000, CTS, #2478; Cell Signaling Technology) antibodies and then stripped with Restore Western Blot Stripping Buffer (Thermo Scientific). .. The membranes were then probed again with anti‐AXL (1:1000, CTS, #8661; Cell Signaling Technology), anti‐H3 (1:1000, CTS, #3638; Cell Signaling Technology), anti‐FLT3 (1:1000, CTS, #3462; Cell Signaling Technology) or anti‐actin (1:1000, #MAB1501; Sigma‐Aldrich) antibodies.



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    R&D Systems paxl y779 antibody
    Pioglitazone incubation and co‐culture with MS‐5 stromal cells enhances AXL activation in OCI‐AML3 cell line and is PPAR‐γ dependent. OCI‐AML3 cell line was co‐cultured with MS‐5 stromal cells and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or a combination of both. (A) Levels of phosphorylated AXL <t>Y779</t> in OCI‐AML3 at day 7 determined by flow cytometry with (B) results expressed by stain index ratio compared with vehicle (DMSO). (C) OCI‐AML3 cell line was co‐cultured with PPAR‐γ KO or Cas9 control MS‐5 stromal cells using Transwell ® inserts with 0.4 μm pore and then treated with pioglitazone (10 μ m ). Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (D) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry. (E) Mouse Gas6 protein levels secreted by wild‐type or PPAR‐γ KO MS‐5 stromal cells were examined when cultured alone or co‐cultured with OCI‐AML3 cell line. (F) Mouse Gas6 protein levels secreted by wild‐type stromal cells, co‐cultured with OCI‐AML3 cell line and treated with pioglitazone (10 μ m ) compared with vehicle (DMSO). Results expression: mean ± SEM of at least three independent experiments with *, P < 0.05; **, P < 0.01; ns, non‐significant.
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    Pioglitazone incubation and co‐culture with MS‐5 stromal cells enhances AXL activation in OCI‐AML3 cell line and is PPAR‐γ dependent. OCI‐AML3 cell line was co‐cultured with MS‐5 stromal cells and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or a combination of both. (A) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry with (B) results expressed by stain index ratio compared with vehicle (DMSO). (C) OCI‐AML3 cell line was co‐cultured with PPAR‐γ KO or Cas9 control MS‐5 stromal cells using Transwell ® inserts with 0.4 μm pore and then treated with pioglitazone (10 μ m ). Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (D) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry. (E) Mouse Gas6 protein levels secreted by wild‐type or PPAR‐γ KO MS‐5 stromal cells were examined when cultured alone or co‐cultured with OCI‐AML3 cell line. (F) Mouse Gas6 protein levels secreted by wild‐type stromal cells, co‐cultured with OCI‐AML3 cell line and treated with pioglitazone (10 μ m ) compared with vehicle (DMSO). Results expression: mean ± SEM of at least three independent experiments with *, P < 0.05; **, P < 0.01; ns, non‐significant.

    Journal: The Febs Journal

    Article Title: The AXL inhibitor bemcentinib overcomes microenvironment‐mediated resistance to pioglitazone in acute myeloid leukemia

    doi: 10.1111/febs.17263

    Figure Lengend Snippet: Pioglitazone incubation and co‐culture with MS‐5 stromal cells enhances AXL activation in OCI‐AML3 cell line and is PPAR‐γ dependent. OCI‐AML3 cell line was co‐cultured with MS‐5 stromal cells and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or a combination of both. (A) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry with (B) results expressed by stain index ratio compared with vehicle (DMSO). (C) OCI‐AML3 cell line was co‐cultured with PPAR‐γ KO or Cas9 control MS‐5 stromal cells using Transwell ® inserts with 0.4 μm pore and then treated with pioglitazone (10 μ m ). Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (D) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry. (E) Mouse Gas6 protein levels secreted by wild‐type or PPAR‐γ KO MS‐5 stromal cells were examined when cultured alone or co‐cultured with OCI‐AML3 cell line. (F) Mouse Gas6 protein levels secreted by wild‐type stromal cells, co‐cultured with OCI‐AML3 cell line and treated with pioglitazone (10 μ m ) compared with vehicle (DMSO). Results expression: mean ± SEM of at least three independent experiments with *, P < 0.05; **, P < 0.01; ns, non‐significant.

    Article Snippet: AXL phosphorylation was analyzed using pAxl Y779 antibody (R&D Systems, Minneapolis, MN, USA) on fixed and permeabilized cells (BD Cytofix/CytopermTM, BD Biosciences, Le Pont de Claix, France).

    Techniques: Incubation, Co-Culture Assay, Activation Assay, Cell Culture, Flow Cytometry, Staining, Control, Expressing

    Exogenous Gas6 addition or MS‐5 conditioned medium mimics stroma‐induced resistance to pioglitazone. (A) OCI‐AML3 cell line was treated with pioglitazone (10 μ m ) alone, exogenous Gas6 (50 ng·mL −1 ) alone or in combination. Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (B) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry with (C) results expressed by stain index ratio compared with vehicle (DMSO). The same color code has been used for (B and C). OCI‐AML3 cell line was cultured in standard medium or MS‐5 conditioned medium (CM) and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or in combination (D). Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (E) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry with results expressed by stain index ratio compared with vehicle (DMSO). (F) Relative mouse Gas6 protein levels assessed by ELISA in conditioned medium at day 7 compared with untreated conditioned medium. The same color code has been used for (E and F). Results expression: mean ± SEM of at least three independent experiments with *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, non‐significant.

    Journal: The Febs Journal

    Article Title: The AXL inhibitor bemcentinib overcomes microenvironment‐mediated resistance to pioglitazone in acute myeloid leukemia

    doi: 10.1111/febs.17263

    Figure Lengend Snippet: Exogenous Gas6 addition or MS‐5 conditioned medium mimics stroma‐induced resistance to pioglitazone. (A) OCI‐AML3 cell line was treated with pioglitazone (10 μ m ) alone, exogenous Gas6 (50 ng·mL −1 ) alone or in combination. Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (B) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry with (C) results expressed by stain index ratio compared with vehicle (DMSO). The same color code has been used for (B and C). OCI‐AML3 cell line was cultured in standard medium or MS‐5 conditioned medium (CM) and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or in combination (D). Cell counts were performed by flow cytometry and compared with vehicle (DMSO). (E) Levels of phosphorylated AXL Y779 in OCI‐AML3 at day 7 determined by flow cytometry with results expressed by stain index ratio compared with vehicle (DMSO). (F) Relative mouse Gas6 protein levels assessed by ELISA in conditioned medium at day 7 compared with untreated conditioned medium. The same color code has been used for (E and F). Results expression: mean ± SEM of at least three independent experiments with *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, non‐significant.

    Article Snippet: AXL phosphorylation was analyzed using pAxl Y779 antibody (R&D Systems, Minneapolis, MN, USA) on fixed and permeabilized cells (BD Cytofix/CytopermTM, BD Biosciences, Le Pont de Claix, France).

    Techniques: Flow Cytometry, Staining, Cell Culture, Enzyme-linked Immunosorbent Assay, Expressing

    Pioglitazone and co‐culture with MS‐5 stromal cells enhance AXL activation in primary AML cells via a PPAR‐γ‐dependent mechanism. Primary AML cells from two different AML patients ( n = 1 for each patient) were co‐cultured with wild type (A, UPN6 and B, UPN7) or PPAR‐γ KO (C, UPN6 and D, UPN7) MS‐5 stromal cells, and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or a combination of both. First plots (left): reduction in cell growth induced in AML primary cells after drug incubation compared with vehicle. Cell counts were performed by flow cytometry. Second and third plots (middle and right): levels of phosphorylated AXL Y779 in AML cells at day 7 determined by flow cytometry and results expressed by stain index ratio compared to vehicle (DMSO).

    Journal: The Febs Journal

    Article Title: The AXL inhibitor bemcentinib overcomes microenvironment‐mediated resistance to pioglitazone in acute myeloid leukemia

    doi: 10.1111/febs.17263

    Figure Lengend Snippet: Pioglitazone and co‐culture with MS‐5 stromal cells enhance AXL activation in primary AML cells via a PPAR‐γ‐dependent mechanism. Primary AML cells from two different AML patients ( n = 1 for each patient) were co‐cultured with wild type (A, UPN6 and B, UPN7) or PPAR‐γ KO (C, UPN6 and D, UPN7) MS‐5 stromal cells, and treated with pioglitazone (10 μ m ) alone, bemcentinib (50 n m ) alone or a combination of both. First plots (left): reduction in cell growth induced in AML primary cells after drug incubation compared with vehicle. Cell counts were performed by flow cytometry. Second and third plots (middle and right): levels of phosphorylated AXL Y779 in AML cells at day 7 determined by flow cytometry and results expressed by stain index ratio compared to vehicle (DMSO).

    Article Snippet: AXL phosphorylation was analyzed using pAxl Y779 antibody (R&D Systems, Minneapolis, MN, USA) on fixed and permeabilized cells (BD Cytofix/CytopermTM, BD Biosciences, Le Pont de Claix, France).

    Techniques: Co-Culture Assay, Activation Assay, Cell Culture, Incubation, Flow Cytometry, Staining