phospho pyk2 Search Results


92
R&D Systems mouse monoclonal antiphosphorylated pyk2
Mouse Monoclonal Antiphosphorylated Pyk2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio-Techne corporation human/mouse/rat catalase antibody
Human/Mouse/Rat Catalase Antibody, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc phospho pyk2 tyr402 cell signaling technology 3291s
Phospho Pyk2 Tyr402 Cell Signaling Technology 3291s, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems phosphorpyk2
Phosphorpyk2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Biorbyt anti phospho protein tyrosine kinase 2 β phospho tyr579
( A ) Representative confocal immunofluorescence staining of Rac1 in HUVECs treated with vehicle (Ctrl) or sortilin alone or pretreated with the S1P3 inhibitor TY52156. Arrows indicate membrane translocation of Rac1. Scale bar: 10 μm. Insets show higher magnification, zoom ×4.7. ( B ) Acetylcholine-evoked vasorelaxation in WT mesenteric arteries exposed to vehicle, sortilin alone, or sortilin in the presence of NSC23766 ( n = 3). ( C ) Acetylcholine-evoked vasorelaxation in WT mesenteric arteries treated with vehicle or sortilin alone or pretreated with either ML171 or GSK2795039 before sortilin stimulation ( n = 3). ( D ) NOX activity in HUVECs treated with vehicle or sortilin alone or preincubated with ML171 or GSK2795039 before sortilin ( n = 4–5 replicates from 3 independent experiments). ( E ) NOX activity in WT and gp91 phox–/– mesenteric arteries exposed to vehicle or sortilin ( n = 3 replicates from 3 independent experiments). Data are expressed as increase of chemiluminescence per minute in arbitrary units. ( F ) Acetylcholine-evoked vasorelaxation in mesenteric arteries from WT and gp91 phox–/– mice exposed to vehicle or sortilin ( n = 5). ( G ) Representative immunoblots and densitometric analyses of 3 independent experiments evaluating protein levels of <t>phospho-Tyr579-PYK2,</t> phospho-Ser729-PKCɛ, phospho-Thr497-PKCα, PKC, S1P3, and Rac1-GTP in HUVECs treated with vehicle or sortilin in the presence or absence of TY52156 or GSK2795039. Data are represented as mean ± SD. One-way ANOVA ( D , E , and G ) or 2-way ANOVA ( B , C , and F ) followed by Bonferroni’s post hoc test was used. ( C ) * P < 0.0001 versus vehicle or GSK2795039 plus sortilin at the same acetylcholine concentration (as indicated by color code).
Anti Phospho Protein Tyrosine Kinase 2 β Phospho Tyr579, supplied by Biorbyt, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Signalway Antibody phospho-pyk2 (tyr-402
Caldecrin inhibits RANKL-stimulated phosphorylation (p-) of c-Src, Syk, and <t>Pyk2</t> in mature OCs. RAW264.7 cells (RAW) or BMMs (BMM) were differentiated into mature OCs in the presence of RANKL or M-CSF and RANKL for 3–4 days and then in medium depleted of RANKL for 12 h. The cells were incubated without (N) or with RANKL alone (R) or RANKL + caldecrin (R + C) for 15 min. Cell lysates (20 μg) were subjected to Western blotting as described under “Experimental Procedures.”
Phospho Pyk2 (Tyr 402, supplied by Signalway Antibody, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


( A ) Representative confocal immunofluorescence staining of Rac1 in HUVECs treated with vehicle (Ctrl) or sortilin alone or pretreated with the S1P3 inhibitor TY52156. Arrows indicate membrane translocation of Rac1. Scale bar: 10 μm. Insets show higher magnification, zoom ×4.7. ( B ) Acetylcholine-evoked vasorelaxation in WT mesenteric arteries exposed to vehicle, sortilin alone, or sortilin in the presence of NSC23766 ( n = 3). ( C ) Acetylcholine-evoked vasorelaxation in WT mesenteric arteries treated with vehicle or sortilin alone or pretreated with either ML171 or GSK2795039 before sortilin stimulation ( n = 3). ( D ) NOX activity in HUVECs treated with vehicle or sortilin alone or preincubated with ML171 or GSK2795039 before sortilin ( n = 4–5 replicates from 3 independent experiments). ( E ) NOX activity in WT and gp91 phox–/– mesenteric arteries exposed to vehicle or sortilin ( n = 3 replicates from 3 independent experiments). Data are expressed as increase of chemiluminescence per minute in arbitrary units. ( F ) Acetylcholine-evoked vasorelaxation in mesenteric arteries from WT and gp91 phox–/– mice exposed to vehicle or sortilin ( n = 5). ( G ) Representative immunoblots and densitometric analyses of 3 independent experiments evaluating protein levels of phospho-Tyr579-PYK2, phospho-Ser729-PKCɛ, phospho-Thr497-PKCα, PKC, S1P3, and Rac1-GTP in HUVECs treated with vehicle or sortilin in the presence or absence of TY52156 or GSK2795039. Data are represented as mean ± SD. One-way ANOVA ( D , E , and G ) or 2-way ANOVA ( B , C , and F ) followed by Bonferroni’s post hoc test was used. ( C ) * P < 0.0001 versus vehicle or GSK2795039 plus sortilin at the same acetylcholine concentration (as indicated by color code).

Journal: The Journal of Clinical Investigation

Article Title: Targeting the ASMase/S1P pathway protects from sortilin-evoked vascular damage in hypertension

doi: 10.1172/JCI146343

Figure Lengend Snippet: ( A ) Representative confocal immunofluorescence staining of Rac1 in HUVECs treated with vehicle (Ctrl) or sortilin alone or pretreated with the S1P3 inhibitor TY52156. Arrows indicate membrane translocation of Rac1. Scale bar: 10 μm. Insets show higher magnification, zoom ×4.7. ( B ) Acetylcholine-evoked vasorelaxation in WT mesenteric arteries exposed to vehicle, sortilin alone, or sortilin in the presence of NSC23766 ( n = 3). ( C ) Acetylcholine-evoked vasorelaxation in WT mesenteric arteries treated with vehicle or sortilin alone or pretreated with either ML171 or GSK2795039 before sortilin stimulation ( n = 3). ( D ) NOX activity in HUVECs treated with vehicle or sortilin alone or preincubated with ML171 or GSK2795039 before sortilin ( n = 4–5 replicates from 3 independent experiments). ( E ) NOX activity in WT and gp91 phox–/– mesenteric arteries exposed to vehicle or sortilin ( n = 3 replicates from 3 independent experiments). Data are expressed as increase of chemiluminescence per minute in arbitrary units. ( F ) Acetylcholine-evoked vasorelaxation in mesenteric arteries from WT and gp91 phox–/– mice exposed to vehicle or sortilin ( n = 5). ( G ) Representative immunoblots and densitometric analyses of 3 independent experiments evaluating protein levels of phospho-Tyr579-PYK2, phospho-Ser729-PKCɛ, phospho-Thr497-PKCα, PKC, S1P3, and Rac1-GTP in HUVECs treated with vehicle or sortilin in the presence or absence of TY52156 or GSK2795039. Data are represented as mean ± SD. One-way ANOVA ( D , E , and G ) or 2-way ANOVA ( B , C , and F ) followed by Bonferroni’s post hoc test was used. ( C ) * P < 0.0001 versus vehicle or GSK2795039 plus sortilin at the same acetylcholine concentration (as indicated by color code).

Article Snippet: Immunoblotting was performed as previously described , using the following antibodies: anti–phospho-eNOS serine 1177 (Enzo Life Sciences, catalog ALX-804-396-C100, clone 15E2); anti-phospho-eNOS-Thr494 (Cell Signaling Technology, catalog 9574); anti-eNOS (Cell Signaling Technology, catalog 9570); anti–β-actin (Abcam, mAb, catalog ab8226, clone mAbcam 8226); anti–phospho-protein-tyrosine kinase 2-β phospho-Tyr579 (PYK2B pY579) (Elabscience, catalog E-AB-21240); anti–phospho-PKCɛ Ser729 (Biorbyt, catalog orb315664); anti–PKCα (phospho T497) antibody (Abcam, catalog ab76016, clone EP2608Y); anti–PKC-PAN (Sigma-Aldrich, catalog SAB4502356); anti-ASMase (SMPD1; Biorbyt, catalog ORB214591); anti-S1P1 (Immunological Sciences, catalog AB-83739); anti-S1P3 (Elabscience, catalog E-AB-31267); anti-gp91phox (Santa Cruz Biotechnology Inc., catalog sc-130543, clone 54.1); anti-SphK1 (Santa Cruz Biotechnology Inc., catalog sc-365401, clone G-11); anti-SphK2 (MyBioSource, catalog MBS2518663); anti-aCDase (ASAH1; MyBioSource, catalog MBS1492517), and anti-active Rac1 (Rac1-GTP) (Neweast Bioscience, catalog 26903).

Techniques: Immunofluorescence, Staining, Translocation Assay, Activity Assay, Western Blot, Concentration Assay

Caldecrin inhibits RANKL-stimulated phosphorylation (p-) of c-Src, Syk, and Pyk2 in mature OCs. RAW264.7 cells (RAW) or BMMs (BMM) were differentiated into mature OCs in the presence of RANKL or M-CSF and RANKL for 3–4 days and then in medium depleted of RANKL for 12 h. The cells were incubated without (N) or with RANKL alone (R) or RANKL + caldecrin (R + C) for 15 min. Cell lysates (20 μg) were subjected to Western blotting as described under “Experimental Procedures.”

Journal: The Journal of Biological Chemistry

Article Title: Serum Calcium-decreasing Factor, Caldecrin, Inhibits Receptor Activator of NF-?B Ligand (RANKL)-mediated Ca 2+ Signaling and Actin Ring Formation in Mature Osteoclasts via Suppression of Src Signaling Pathway *

doi: 10.1074/jbc.M112.358796

Figure Lengend Snippet: Caldecrin inhibits RANKL-stimulated phosphorylation (p-) of c-Src, Syk, and Pyk2 in mature OCs. RAW264.7 cells (RAW) or BMMs (BMM) were differentiated into mature OCs in the presence of RANKL or M-CSF and RANKL for 3–4 days and then in medium depleted of RANKL for 12 h. The cells were incubated without (N) or with RANKL alone (R) or RANKL + caldecrin (R + C) for 15 min. Cell lysates (20 μg) were subjected to Western blotting as described under “Experimental Procedures.”

Article Snippet: Samples were separated by SDS-PAGE, transferred onto Immobilon-P PVDF membranes (Millipore, Billerica, MA), and then immunoblotted with antibody against Akt, phospho-Akt (Ser-473), phospho-Syk (Tyr-525/526), PLCγ1, phospho-PLCγ1 (Tyr-783), PLCγ2, phospho-PLCγ2 (Tyr-1217), Src homology 2 domain-containing leukocyte protein (SLP)-76, ERK, phospho-ERK (Thr-202/Tyr-204), JNK, phospho-JNK (Thr-183/Tyr-185) (Cell Signaling Technology, Danvers, MA), c-Src (Santa Cruz Biotechnology, Inc. (Santa Cruz, CA), Cell Signaling Technology, and R&D Systems), phospho-Src (p-Src) (human Tyr(P)-418 corresponding to mouse Tyr(P)-416; Invitrogen), Syk (N-19; Santa Cruz Biotechnology), phospho-SLP-76 (Tyr-128; Assay Biotechnology Co., Sunnyvale, CA), Pyk2 (BD Transduction Laboratories Inc., Lexington, KY), phospho-Pyk2 (Tyr-402; Signalway Antibody, Pearland, TX), or β-actin (Medical and Biological Laboratories, Nagoya, Japan).

Techniques: Incubation, Western Blot

Model for RANKL-induced actin ring organization in mature OCs. RANKL-RANK binding causes recruitment of TRAF6 to RANK. TRAF6 initiates downstream activation of NF-κB, JNK, ERK, and Akt. TRAF6 also activates c-Src and c-Src·Syk complex localized in integrin and ITAM. Activated Syk phosphorylates PLCγ via SLP-76, which leads to activation of TRPV4 channels and evokes Ca2+ influx. Increased Ca2+ activates Pyk2 and associates with Src, leading to cytoskeletal organization. Caldecrin inhibits TRAF6-mediated c-Src phosphorylation, thereby inhibiting bone resorption regulated by Ca2+ influx and organization of the actin cytoskeleton.

Journal: The Journal of Biological Chemistry

Article Title: Serum Calcium-decreasing Factor, Caldecrin, Inhibits Receptor Activator of NF-?B Ligand (RANKL)-mediated Ca 2+ Signaling and Actin Ring Formation in Mature Osteoclasts via Suppression of Src Signaling Pathway *

doi: 10.1074/jbc.M112.358796

Figure Lengend Snippet: Model for RANKL-induced actin ring organization in mature OCs. RANKL-RANK binding causes recruitment of TRAF6 to RANK. TRAF6 initiates downstream activation of NF-κB, JNK, ERK, and Akt. TRAF6 also activates c-Src and c-Src·Syk complex localized in integrin and ITAM. Activated Syk phosphorylates PLCγ via SLP-76, which leads to activation of TRPV4 channels and evokes Ca2+ influx. Increased Ca2+ activates Pyk2 and associates with Src, leading to cytoskeletal organization. Caldecrin inhibits TRAF6-mediated c-Src phosphorylation, thereby inhibiting bone resorption regulated by Ca2+ influx and organization of the actin cytoskeleton.

Article Snippet: Samples were separated by SDS-PAGE, transferred onto Immobilon-P PVDF membranes (Millipore, Billerica, MA), and then immunoblotted with antibody against Akt, phospho-Akt (Ser-473), phospho-Syk (Tyr-525/526), PLCγ1, phospho-PLCγ1 (Tyr-783), PLCγ2, phospho-PLCγ2 (Tyr-1217), Src homology 2 domain-containing leukocyte protein (SLP)-76, ERK, phospho-ERK (Thr-202/Tyr-204), JNK, phospho-JNK (Thr-183/Tyr-185) (Cell Signaling Technology, Danvers, MA), c-Src (Santa Cruz Biotechnology, Inc. (Santa Cruz, CA), Cell Signaling Technology, and R&D Systems), phospho-Src (p-Src) (human Tyr(P)-418 corresponding to mouse Tyr(P)-416; Invitrogen), Syk (N-19; Santa Cruz Biotechnology), phospho-SLP-76 (Tyr-128; Assay Biotechnology Co., Sunnyvale, CA), Pyk2 (BD Transduction Laboratories Inc., Lexington, KY), phospho-Pyk2 (Tyr-402; Signalway Antibody, Pearland, TX), or β-actin (Medical and Biological Laboratories, Nagoya, Japan).

Techniques: Binding Assay, Activation Assay