Phospho-PDGFRB (Tyr740) Antibody
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Product Specs
Form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Lead Time
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Synonyms
Beta platelet derived growth factor receptor antibody; Beta-type platelet-derived growth factor receptor antibody; CD 140B antibody; CD140 antigen-like family member B antibody; CD140b antibody; CD140b antigen antibody; IBGC4 antibody; IMF1 antibody; JTK12 antibody; OTTHUMP00000160528 antibody; PDGF R beta antibody; PDGF Receptor beta antibody; PDGF-R-beta antibody; PDGFR 1 antibody; PDGFR antibody; PDGFR beta antibody; PDGFR1 antibody; PDGFRB antibody; PGFRB_HUMAN antibody; Platelet derived growth factor receptor 1 antibody; Platelet derived growth factor receptor beta antibody; Platelet derived growth factor receptor beta polypeptide antibody
Target Names
Uniprot No.
Target Background
Function
Tyrosine-protein kinase that functions as a cell-surface receptor for homodimeric PDGFB and PDGFD, as well as for heterodimers formed by PDGFA and PDGFB. This receptor plays a critical role in regulating embryonic development, cell proliferation, survival, differentiation, chemotaxis, and migration. It is particularly important for blood vessel development, promoting proliferation, migration, and recruitment of pericytes and smooth muscle cells to endothelial cells. Additionally, it contributes to the migration of vascular smooth muscle cells and the formation of neointima at vascular injury sites. PDGFRB is essential for normal development of the cardiovascular system and is required for the proper recruitment of pericytes (mesangial cells) in the kidney glomerulus and for the formation of a branched network of capillaries in kidney glomeruli. It facilitates the rearrangement of the actin cytoskeleton and the formation of membrane ruffles. Binding of its cognate ligands - homodimeric PDGFB, heterodimers formed by PDGFA and PDGFB, or homodimeric PDGFD - leads to the activation of various signaling cascades. The response elicited depends on the nature of the bound ligand and is modulated by the formation of heterodimers between PDGFRA and PDGFRB. PDGFRB phosphorylates PLCG1, PIK3R1, PTPN11, RASA1/GAP, CBL, SHC1, and NCK1. Activation of PLCG1 results in the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate, mobilization of cytosolic Ca(2+), and the activation of protein kinase C. Phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, activates the AKT1 signaling pathway. Phosphorylation of SHC1, or of the C-terminus of PTPN11, creates a binding site for GRB2, leading to the activation of HRAS, RAF1, and downstream MAP kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. PDGFRB promotes phosphorylation and activation of SRC family kinases and facilitates the phosphorylation of PDCD6IP/ALIX and STAM. Receptor signaling is downregulated by protein phosphatases that dephosphorylate the receptor and its downstream effectors, and by rapid internalization of the activated receptor.
Gene References Into Functions
- EBF1-PDGFRB is sufficient to drive leukemogenesis. PMID: 28555080
- A study demonstrated that LRIG2 promotes PDGFRB-induced proliferation of glioblastoma multiforme cells in vitro and in vivo through regulating PDGFRB signaling-mediated cell cycle progression. PMID: 30015847
- High expression of PDGFR-beta in prostate cancer stroma is independently associated with clinical and biochemical prostate cancer recurrence. PMID: 28233816
- A study investigated the more detailed mechanism for the cis-interaction of Necl-5 with the PDGF receptor beta. Necl-5 contains three Ig-like domains and the PDGF receptor beta contains five Ig-like domains at their extracellular regions. The study demonstrated that the third Ig-like domain of Necl-5 cis-interacted with the fifth Ig-like domain of the PDGF receptor beta. PMID: 29431243
- A study revealed that high PDGFRbeta expression in cancer tissue was an independent marker of poor prognosis relating to recurrence in patients with colorectal cancer. PMID: 29498405
- Melatonin reinforces the anticancer activity of sorafenib by downregulation of PDGFR-beta/STAT3 signaling pathway and melatonin receptor (MT)-mediated STAT3. PMID: 29953970
- High GLI2 or PDGFRB expression is associated with unfavorable survival in GC patients. GLI2 can induce PDGFRB expression in GC cells via directly binding to its promoter. Additionally, the GLI2-PDGFRB axis might be an important signaling pathway modulating CSC properties of GC cells. PMID: 28975979
- The cell surface PDGFRB is a major link between high glucose and its effectors Hif1a and TGFB for induction of diabetic mesangial cell hypertrophy. PMID: 28951244
- This study describes three unique PDGFRB fusions in childhood B- or T-ALL. All three PDGFRB fusion partners have previously been reported to be implicated in hematopoiesis and immune responses. PMID: 28552906
- These findings indicate that miR-518b may function as a tumor suppressor by targeting PDGFRB in the occurrence and development of GBM. PMID: 28849154
- Data show that an equilibrium mixture of two unusual end-insertion G-quadruplexes forms in a native promoter sequence and appears to be the molecular recognition for platelet derived growth factor receptor beta (PDGFR-beta) downregulation. PMID: 29288770
- Case Report: heterozygous PDGFRB mutation in a family presenting with multicentric autosomal dominant infantile myofibromatosis. PMID: 28417142
- Anlotinib inhibits the activation of VEGFR2, PDGFRbeta and FGFR1 as well as their common downstream ERK signaling. PMID: 29454091
- PDGFRB is not a major causative gene of primary familial brain calcification in the Chinese population. PMID: 28298627
- These findings indicate that the levels of phosphorylated PDGFR-beta are decreased in endothelial progenitor cells with the in vitro expansion process, which impairs their angiogenic potential by inhibiting PI3K/Akt signaling. PMID: 28487975
- This review showed that PDGFRB was one of the common genes involved with brain calcification. PMID: 28162874
- Data indicate a positive association between LETM1 up-regulation, YAP1 nuclear localization and high PDGFB expression. PMID: 27556512
- This is the first report of a Korean family that carries a PDGFRB mutation potentially responsible for supernumerary premolars. Our results demonstrate the power of next-generation sequencing in rapidly determining the genetic aetiology of numerical tooth abnormalities. PMID: 28393601
- Genetic analyses indicated a platelet derived growth factor receptor beta (PDGFRB) gene missense heterozygous germline mutation in a newborn boy, and his sister suffered from a skull base tumor with the same genotype and histology. PMID: 28183292
- Here we report on a special case of a Ph-like acute lymphoblastic leukemia patient who had a variant ATF7IP/PDGFRB fusion. In this case, a variant fusion was created between ATF7IP exon 9 (instead of exon 13) and PDGFRB exon 11, resulting in the loss of 411 nucleotides and 137 amino acids in the ATF7IP/PDGFRB fusion cDNA and its encoded chimeric protein, respectively. PMID: 29133777
- Data show that MLLT11/AF1q-induced PDGFR signaling enhanced STAT3 activity through Src kinase activation. PMID: 27259262
- In conclusion, a specific class of mutations in PDGFRB causes a clinically recognizable syndromic form of skeletal overgrowth. PMID: 28639748
- The study suggests the association of activation of Akt-mTOR pathway proteins and PDGFR-beta in fibrosarcomatous transformation of dermatofibrosarcoma protuberans. PMID: 28711648
- High PDGFRB expression is associated with gastric cancer. PMID: 28423550
- Authors identified gain-of-function PDGFRB mutations in the majority of multifocal infantile myofibromatosis cases, shedding light on the mechanism of disease development, which is reminiscent of multifocal venous malformations induced by TIE2 mutations. PMID: 28334876
- Findings not only confirm the important role of R853 in establishing the resistant phenotype of the mutant NDEL1-PDGFRB, but also underline the potential of protein modelling for prediction of sensitivity and resistance to TKI treatment. PMID: 27573554
- A novel mutation in PDGFRB [NM_002609.3:c.1699A > G, p.Lys567Glu] was identified in infantile myofibromatosis patients. PMID: 28286173
- Identify PDGFRbeta as a driver in activating Akt/mTORC1 nexus for high glucose-mediated expression of collagen I (alpha2) in proximal tubular epithelial cells, which contributes to tubulointerstitial fibrosis in diabetic nephropathy. PMID: 28424212
- Higher expression of PDGFR-Beta is related to more serious dural penetration of clival chordomas. PMID: 27506406
- Targeted next-generation DNA sequencing identified PDGFRB alterations in all cases of myopericytomatosis and conventional myopericytoma tested (5 cases each), including mutations in 4 cases of myopericytomatosis (N666K in 3; Y562-R565 deletion in 1 case) and 3 myopericytomas (Y562C, K653E, and splice acceptor deletion in 1 case each), as well as low-level PDGFRB amplification in 2 cases of myopericytomatosis and 4 myoperi PMID: 28505006
- Elevated PDGFRB expression was noted in 20.7% of patients with papillary renal cell carcinoma. PMID: 27989785
- Imatinib in myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRB in chronic or blast phase PMID: 28725989
- Inhibition of any internalization mechanism impaired activation of STAT3 but not of other downstream effectors of PDGFRbeta. PMID: 27980069
- This is the first study reporting apparently somatic recurrent PDGFRB mutations as molecular driver events in the majority of sporadic infantile and adult solitary myofibromas PMID: 27776010
- Results demonstrate that miR-9 and miR-200 play opposite roles in the regulation of the vasculogenic ability of triple-negative breast cancer, acting as facilitator and suppressor of PDGFRbeta, respectively. PMID: 27402080
- Among 15 childhood ALL patients with EBF1-PDGFRB fusion proteins, the fusion arose from interstitial deletion of 5q33 (n = 11), balanced rearrangement (n = 2), or complex rearrangement (n = 2). PMID: 26872634
- Previously unrecognised associations between renal cell carcinoma survival and the absolute levels, and variability, of perivascular PDGFR-beta. PMID: 27931046
- This study suggested that the epithelial-mesenchymal transition process can be triggered by the PDGF-D/PDGFRb axis in tongue squamous cell carcinoma, and then involved in the tumor cell invasion via activation of p38/AKT/ERK/ epithelial-mesenchymal transition pathway. PMID: 27507215
- That a loss of KAI1/CD82 and an increase in PDGFR expression in gliomas relate to progressive tumor growth. PMID: 27764516
- Identified PDGFRbeta as a novel marker of stromal activation in oral squamous cell carcinoma. PDGFRbeta was found to be the highest-ranking receptor protein genome-wide. PMID: 27128408
- PDGFR-positive myeloid neoplasms are rare. Marked leukocytosis with marked eosinophilia has been rarely described in myeloid neoplasms associated with PDGFR rearrangement. PMID: 28209946
- Stromal expression of PDGFRbeta increased with increasing histologic grade of breast phyllodes tumor. PDGFR stromal positivity was associated with shorter overall survival. PMID: 27881889
- The expression level of PDGFRB in glioblastoma multiforme pericytes from the microvascular proliferation was significantly higher than that in GBM tumor cells. miRNAs targeting PDGFRB were downregulated in microvascular proliferation. PMID: 26857280
- PDGFRB gene rearrangement is associated with transformation from atypical chronic myeloid leukemia to chronic myelomonocytic leukemia. PMID: 26881541
- Results suggested that increased bFGF upregulates the expression of PDGFRbeta and may enhance PDGFRbeta-mediated pericyte functions after brain ischemia. PMID: 26569132
- Data suggest that cross-talk between PDGFb-dependent beta-catenin activation and Wnt signaling increases pulmonary artery smooth muscle cell proliferation in idiopathic pulmonary arterial hypertension. Proliferation is not increased in normal cells. PMID: 26787464
- The KIT and PDGFRB mutations were predicted to be pathogenic using in silico analysis, whereas the ERBB2 mutation was predicted to be benign. The patient was treated with pazopanib and achieved a partial response that lasted for 7.5 months. PMID: 26483058
- These molecular insights confirm that mutant PDGFRB is indeed the driver mutation in PDGFRB rearranged myeloid neoplasms, consistent with the robust treatment responses with imatinib. PMID: 26662677
- PDGFs could exert their mechanism of action through an autocrine/paracrine effect on granulosa and theca cells mediated by PDGFRs. PMID: 25937181
- Soluble platelet-derived growth factor receptor-beta is a biomarker of brain pericyte injury and blood-brain barrier dysfunction. PMID: 26407747
Database Links
Involvement In Disease
Myeloproliferative disorder chronic with eosinophilia (MPE); Leukemia, acute myelogenous (AML); Leukemia, juvenile myelomonocytic (JMML); Basal ganglia calcification, idiopathic, 4 (IBGC4); Myofibromatosis, infantile 1 (IMF1); Kosaki overgrowth syndrome (KOGS); Premature aging syndrome, Penttinen type (PENTT)
Protein Families
Protein kinase superfamily, Tyr protein kinase family, CSF-1/PDGF receptor subfamily
Subcellular Location
Cell membrane; Single-pass type I membrane protein. Cytoplasmic vesicle. Lysosome lumen. Note=After ligand binding, the autophosphorylated receptor is ubiquitinated and internalized, leading to its degradation.
Q&A
What experimental controls are essential when detecting PDGFRβ phosphorylation at Tyr740?
Phospho-specific antibodies require rigorous validation to avoid false-positive signals. Key controls include:
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Kinase-inactive PDGFRβ mutants: Cells expressing kinase-dead receptors (e.g., Lys634Arg mutation) should show no phosphorylation at Tyr740 upon PDGF stimulation, as autophosphorylation is abolished .
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Peptide competition assays: Pre-incubate the antibody with its immunogen peptide (e.g., residues 711-760 surrounding Tyr740 ). Validated antibodies will show >90% signal reduction in western blotting (WB) .
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Phosphatase treatment: Lysates treated with λ-phosphatase should eliminate the target band, confirming phosphorylation dependency .
Table 1: Control Experiments for Antibody Validation
| Control Type | Expected Result (WB) | Supporting Evidence |
|---|---|---|
| Knockout cell lysates | No band at ~170-190 kDa | |
| Phosphatase-treated lysates | Complete signal loss | |
| Competing peptide | ≥90% signal reduction |
How do I optimize western blot conditions for phospho-PDGFRβ (Tyr740)?
Critical parameters include:
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Gel percentage: Use 7.5–10% SDS-PAGE to resolve the 170–190 kDa receptor .
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Blocking buffer: 5% BSA in TBST reduces non-specific binding compared to milk-based blockers .
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Antibody dilution: Start with 1:1,000 in WB; adjust based on signal-to-noise ratios (e.g., 1:500 for low-abundance targets ).
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Activation timecourse: PDGF-BB stimulation typically peaks at 10–15 min; delayed harvesting may miss transient phosphorylation .
How does Tyr740 phosphorylation interface with PI3K/Akt signaling?
Tyr740 and Tyr751 form a bipartite binding site for the p85 subunit of PI3K. Mutation studies reveal:
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Dual tyrosine requirement: Phe substitutions at both Tyr740 and Tyr751 (F740/751 mutant) abolish PI3K recruitment, preventing PDGF-induced PTEN oxidation and Akt phosphorylation .
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Downstream crosstalk: Cells expressing F740/751 show intact MAPK activation but defective chemotaxis, implicating Tyr740 in pathway-specific signaling .
Table 2: Functional Consequences of PDGFRβ Tyrosine Mutations
| Mutation | PI3K Binding | Akt Phosphorylation | PTEN Oxidation |
|---|---|---|---|
| Wild-type | Yes | Yes | Yes |
| F740/751 | No | No | No |
| Y740/751* | Yes | Yes | Yes |
*Y740/751: Mutant retaining Tyr740/751 but lacking other tyrosines .
How should I resolve conflicting data between phospho-Tyr740 antibodies from different vendors?
Contradictions often arise from epitope masking or cross-reactivity. Mitigation strategies:
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Epitope mapping: Compare immunogen sequences. For example, antibodies raised against residues 711-760 vs. shorter peptides (e.g., GGYMD ) may exhibit differential sensitivity to adjacent post-translational modifications.
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Orthogonal validation: Confirm phosphorylation via:
What methods establish species cross-reactivity for phospho-Tyr740 antibodies?
While many antibodies claim reactivity across human, mouse, and rat , empirical validation is critical:
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Sequence alignment: Verify conservation of the epitope region (e.g., human vs. mouse PDGFRβ Tyr740 flanking sequences are 100% identical ).
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Functional testing: Stimulate primary cells (e.g., mouse fibroblasts, rat vascular smooth muscle cells) with PDGF and compare phosphorylation kinetics to human cell lines .
How can I investigate tyrosine phosphorylation dynamics in live cells?
Combine phospho-specific antibodies with real-time biosensors:
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FRET-based reporters: Genetically encoded sensors (e.g., PDGFRβ-FLARE) enable live-cell imaging of Tyr740 phosphorylation .
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Pharmacological inhibition: Pre-treat cells with PI3K inhibitors (LY294002) to dissect feedback mechanisms affecting phosphorylation persistence .
Methodological Recommendations
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Signal quantification: Normalize phospho-Tyr740 signals to total PDGFRβ levels to account for receptor expression variability .
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Fixation for IHC: Use 4% PFA without methanol to preserve phosphorylation epitopes; avoid Triton X-100 permeabilization, which may extract membrane-bound receptors .
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Data interpretation caveats: Tyr740 phosphorylation is transient (peak at 10 min post-stimulation) and inversely correlates with receptor internalization .
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