Antibody data
- Antibody Data
- Antigen structure
- References [3]
- Comments [0]
- Validations
- Flow cytometry [1]
- Other assay [1]
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- Product number
- 50-9034-42 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- Phospho-SRC (Tyr418) Monoclonal Antibody (SC1T2M3), eFluor™ 660, eBioscience™
- Antibody type
- Monoclonal
- Antigen
- Other
- Description
- Description: This SC1T2M3 monoclonal antibody recognizes human and mouse Src tyrosine kinase (also known as ASV, c-src, c-SRC, p60-Src, pp60c-src, Proto-oncogene c-Src, Proto-oncogene tyrosine-protein kinase Src, SRC1) when phosphorylated on tyrosine 418 (Y418). Autophosphorylation of Src at Y418 in the catalytic domain is required for full catalytic activity of this kinase. Src is a non-receptor tyrosine kinase involved in signal transduction in numerous biological systems and is activated following engagement of many different classes of cellular receptors including immune response receptors, integrins and other adhesion receptors, receptor protein tyrosine kinases, G protein-coupled receptors as well as cytokine receptors. Aberrant Src activity has been implicated in the development of numerous types of cancer. Due to the sequence homology surrounding Src Y418, this SC1T2M3 clone is predicted to cross-react with many Src family kinases including Src, Lck, Fyn, and Lyn.
- Antibody clone number
- SC1T2M3
- Concentration
- 5 µL/Test
Submitted references IL-15 negatively regulates curdlan-induced IL-23 production by human monocyte-derived dendritic cells and subsequent Th17 response.
Analysis of the Human Kinome and Phosphatome by Mass Cytometry Reveals Overexpression-Induced Effects on Cancer-Related Signaling.
Hyperreactivity of junctional adhesion molecule A-deficient platelets accelerates atherosclerosis in hyperlipidemic mice.
Eken A, Okus Z, Erdem S, Azizoglu ZB, Haliloglu Y, Bicer A, Gur TN, Yilmaz E, Karakukcu M, Altuntas HD, Canatan H
Northern clinics of Istanbul 2019;6(4):379-387
Northern clinics of Istanbul 2019;6(4):379-387
Analysis of the Human Kinome and Phosphatome by Mass Cytometry Reveals Overexpression-Induced Effects on Cancer-Related Signaling.
Lun XK, Szklarczyk D, Gábor A, Dobberstein N, Zanotelli VRT, Saez-Rodriguez J, von Mering C, Bodenmiller B
Molecular cell 2019 Jun 6;74(5):1086-1102.e5
Molecular cell 2019 Jun 6;74(5):1086-1102.e5
Hyperreactivity of junctional adhesion molecule A-deficient platelets accelerates atherosclerosis in hyperlipidemic mice.
Karshovska E, Zhao Z, Blanchet X, Schmitt MM, Bidzhekov K, Soehnlein O, von Hundelshausen P, Mattheij NJ, Cosemans JM, Megens RT, Koeppel TA, Schober A, Hackeng TM, Weber C, Koenen RR
Circulation research 2015 Feb 13;116(4):587-99
Circulation research 2015 Feb 13;116(4):587-99
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Intracellular staining of mouse spleen cells untreated (orange histogram) or treated with staurosporine for 2 hours (purple histogram) with Anti-Human/Mouse pSRC (Y418) eFluor® 660 using the Intracellular Fixation & Permeabilization Buffer Set (Product # 88-8824-00) and protocol. Cells in the lymphocyte gate were used for analysis.
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 1 Kinome- and Phosphatome-wide Screen for Effects of Protein Abundance on Signaling States and Dynamics (A) The experimental workflow: ORFs of 541 human kinases and 108 human phosphatases were cloned into a vector encoding GFP-tagged fusion proteins upon transient transfection into HEK293T cells. Cells with or without 10-min EGF stimulation were harvested, barcoded, and stained with antibody mix before mass-cytometry-based single-cell analysis. (B) Plot of counts versus BP-R 2 values for control and experimental samples. Cutoff value was determined by analysis of the BP-R 2 values in all of the control samples. Square-root transformation was applied on the y axis. (C) Venn diagram showing the quantification of POIs with abundance-dependent influences on the AKT pathway (p-PDK1, p-GSK3beta, beta-catenin, p-mTOR, p-p70S6K, p-4EBP1, and p-S6), MAPK-ERK pathways (p-RAF, p-MEK1/2, p-ERK1/2, p-p90RSK, p-CREB, and p-SMAD2/3), stress response pathways (p-MKK3/6, p-MKK4/7, p-p38, p-JNK, p-MAPKAPK2, p-AMPKalpha, and p-p53), and PKC and STAT pathways (grouped for illustration purposes; p-SRC, p-FAK, p-BTK, p-PLCgamma2, p-MARCKS, p-NFkappaB, p-STAT1, p-STAT3, and p-STAT5). (D) Shape-based clustering on all strong signaling.