anti-PDGFRB (PDGFRB) Antikörper

Mouse (Murine) Platelet-Derived Growth Factor Receptor, beta Polypeptide (PDGFRB) Interaktionspartner

1. Inactivation of MAP3K7 in FOXD1-expressing cells results in loss of mesangial PDGFRBeta and juvenile kidney scarring.

2. the tyrosine phosphatase Shp-2 to be the master regulator of Pdgfr phosphotyrosine signaling.

3. PDGFR signaling is necessary for postnatal tendon growth and remodeling and MT1-MMP is a critical mediator of tendon fibroblast migration.

4. PDGFR alpha beta and PDGFR beta beta dimers were strong inducers of random and directionally-persistent migration in mouse skin fibroblast, respectively, that was sustained for up to 24 h.

5. PDGFRbeta was activated around the injury site after experimental traumatic brain injury (TBI), and primarily expressed in astrocytes, microglia, OPC and leukocytes in the boundary of the lesion site, suggesting PDGFRbeta was involved in glial scar formation. Then the PDGFR inhibitor (AG1296) was administered following TBI. Reactive astrocytes were significantly inhibited in AG1296-treated mice.

6. Increasing the adipogenic capacity of Pdgfrbeta(+) precursors through Pparg overexpression results in healthy visceral white adipose tissue expansion in obesity and adiponectin-dependent improvements in glucose homeostasis.

7. PDGFRalpha/PDGFRbeta signaling balance determines progenitor commitment to beige (PDGFRalpha) or white (PDGFRbeta) adipogenesis.

8. The data of this study revealed an acute accumulation of PDGFRbeta+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRbeta-signaling in blood vessel and post-injury tissue recovery.

9. Ltbp4 regulates Pdgfrb expression via TGFbeta-dependent modulation of Nrf2 transcription factor function.

10. Beta platelet-derived growth factor is induced in hepatic stellate cells (HSCs) following surgical partial hepatectomy, and its deletion in HSCs leads to prolonged liver injury in mice. However, there is no significant difference in liver regeneration.

11. The results provide functional evidence that elevated PDGFRbeta signaling causes tissue wasting or overgrowth reminiscent of human genetic syndromes and that the STAT1 pathway is a crucial modulator of this phenotypic spectrum.

12. 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.

13. Data show that three platelet-derived growth factor receptor beta (PDGFRB) mutants (R561C, P660T and N666K) were able to transform NIH3T3 and Ba/F3 cells to different extents.

14. data therefore collectively suggest that upon TGFbeta stimulation, SP1 recruits SMAD2 to the promoter of Pdgfrb to up-regulate its expression and thus Pdgfrb is a direct downstream target of the TGFbeta/SMAD2 signaling

15. PdgfrbetaF7/F7 mice between 4-6 and 36-48 weeks of age developed a region-dependent loss in pericyte coverage (22-46, 24-44 and 4-31%) and cell numbers (36-49, 34-64 and 11-36%), reduction in capillary length (20-39, 13-46 and 1-30%), and an increase in extravascular fibrinogen-derived deposits (3.4-5.2, 2.8-4.1 and 0-3.6-fold) demonstrating BBB breakdown in the cortex, hippocampus and thalamus, respectively.

16. PDGF-B-PDGFRbeta signaling plays a significant role in the development of adipose tissue neovascularization.

17. there is great possibility that EPCs overexpressing PDGFR-beta enhanc VSMC apoptosis and suppress VSMC migration by competitive consumption of PDGF-BB in the early phase after carotid artery injury in mice.

18. PDGFRalpha and PDGFRbeta are coexpressed in the craniofacial mesenchyme of mid-gestation mouse embryos and that ablation of Pdgfrb in the neural crest lineage results in increased nasal septum width, delayed palatal shelf development, and subepidermal blebbing.

19. The results from this study indicate that PDGF signaling is required for fiber hypertrophy, extracellular matrix production, and angiogenesis that occur during muscle growth.

20. Data show that oligodendrocyte transcription factor 2 (Olig2) deletion causes platelet-derived growth factor receptor (PDGFR) downregulation and reciprocal epidermal growth factor receptor (EGFR) upregulation.

Human Platelet-Derived Growth Factor Receptor, beta Polypeptide (PDGFRB) Interaktionspartner

1. Based on expression of platelet-derived growth factor receptor-beta (PDGFR-beta).

2. Recurrent PDGFRB mutations are associated with unicentric Castleman disease.

3. The hypomethylated gene, NRP1, and its co-expressed gene, PDGFRB, were significantly correlated with tumor malignant phenotypes.

4. The CD146 regulates PDGF-B/PDGFRbeta signaling in a multifaceted manner, involving CD146-PDGFRbeta binding, CD146 dimerization, PI3K recruitment, and CD146-cytoskeleton binding.

5. These findings reveal a novel regulatory role of JAK2-mediated PDGFRbeta proteolysis in triple negative breast cancer

6. we describe a complex clonal evolution pattern in Ph-like ALL and identified a novel PDGFRB point mutation that drives leukemia relapse after ABL TKI treatment.

7. Our study confirms that PDGFRB mutation carriers in general have a mild clinical phenotype, and basal ganglia calcifications can be detected by a CT scan, also in asymptomatic mutation carriers

8. In the nucleus, PDGFRbeta formed ligand-inducible complexes with the tyrosine kinase Fer and its substrate, TATA element-modifying factor 1 (TMF-1).

9. Cytogenetically cryptic ZMYM2-FLT3 and DIAPH1-PDGFRB gene fusions in myeloid neoplasms with eosinophilia.

10. Protein expression of tumour and/or stromal cell PDGFRalpha, PDGFRbeta and PDGF-CC was evaluated in primary tumours (N = 489), synchronous lymph node metastases (N = 135) and asynchronous recurrences (N = 39) using immunohistochemistry in a prospectively maintained cohort of primary breast cancer patients

11. Case Reports: PDGFRB mutation in premature ageing syndrome, Penttinen type.

12. EBF1-PDGFRB is sufficient to drive leukemogenesis.

13. Study demonstrated that LRIG2 promoted the PDGFRBinduced proliferation of glioblastoma multiforme cells in vitro and in vivo through regulating the PDGFRB signalingmediated cell cycle progression.

14. High expression of PDGFR-beta in prostate cancer stroma is independently associated with clinical and biochemical prostate cancer recurrence.

15. Study investigated the more detailed mechanism for this 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; showed that the third Ig-like domain of Necl-5 cis-interacted with the fifth Ig-like domain of the PDGF receptor beta.

16. Study revealed that high PDGFRbeta expression in cancer tissue was an independent marker of poor prognosis relating to recurrence in patients with colorectal cancer.

17. Melatonin reinforces the anticancer activity of sorafenib by downregulation of PDGFR-beta/STAT3 signaling pathway and melatonin receptor (MT)-mediated STAT3.

18. 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. In addition, the GLI2-PDGFRB axis might be an important signaling pathway modulating CSC properties of GC cells.

19. The cell surface PDGFRB is a major link between high glucose and its effectors Hif1a and TGFB for induction of diabetic mesangial cell hypertrophy.

20. 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