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anti-Rat (Rattus) PDGFC Anticorps:
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Human Polyclonal PDGFC Primary Antibody pour IHC (p), ELISA - ABIN188196
Kilvaer, Valkov, Sorbye, Donnem, Smeland, Bremnes, Busund: Platelet-Derived Growth Factors in Non-GIST Soft-Tissue Sarcomas Identify a Subgroup of Patients with Wide Resection Margins and Poor Disease-Specific Survival. dans Sarcoma 2011
Show all 2 Pubmed References
Human Polyclonal PDGFC Primary Antibody pour IF (p), IHC (p) - ABIN714566
Hurley, Adams, Wang, Jiang, Meo Burt, Du, Xiao: Accelerated Fracture Healing in Transgenic Mice Overexpressing an Anabolic Isoform of Fibroblast Growth Factor 2. dans Journal of cellular biochemistry 2015
paracrine crosstalk between cancer cells expressing platelet-derived growth factor (PDGF)-CC and cancer-associated fibroblasts expressing the cognate receptors in human basal-like mammary carcinomas, was identified.
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
There are four platelet-derived growth factor (PDGF) genes (PDGFA, PDGFB, PDGFC and PDGFD) that reside on chromosomes 7, 22, 4 and 11.
We conclude that PDGF-CC-induced blood-spinal cord barrier dysfunction can contribute to timing of amyotrophic lateral sclerosis onset
High glucose-mediated induction of PDGF-C via ChREBP in mesangial cells contributes to the development of glomerular mesangial expansion in diabetes.
PDGF-C up-regulation was mediated by the human embryonic lethal abnormal vision-like protein HuR, which stabilizes the PDGF-C transcript by binding to two predicted AU-rich elements (AREs) in the 3'-untranslated region (3'-UTR).
Concomitant upregulation of PDGF-C with VEGF in Glioblastoma tumor cells.
The results indicate that PDGF-C upregulation and calpain-3 downregulation are involved in the aggressiveness of malignant melanoma and suggest that modulators of these proteins
Platelet-derived growth factor-C (PDGF-C) induces anti-apoptotic effects on macrophages through Akt and Bad phosphorylation.
Data indicate uPA (plau) and PAI1 (Serpine1) were up-regulated in human PDGF-C Tg mice, suggesting that uPA could be compensating for the loss of tissue-type plasminogen activator (tPA) activity in PDGF-C Tg; tpa KO mice.
High PDGF-C expression induces progressive fibrosis, chronic inflammation, neoangiogenesis and sinusoidal congestion resulting in hepatocellular carcinoma.
PDGF-C is both angiogenic and a neuronal survival factor, and it is an important component of neurovascular crosstalk. [Review]
Results indicate that the alpha-SMA inducing effect of M2 macrophages is in part mediated by secretion of PGDF-CC.
Single nucleotide polymorphisms in the PDGF-C gene are linked to the development of oral clefts.
Platelet-derived growth factor-C (PDGF-C) activation by serine proteases.
Melanoma cell-derived platelet-derived growth factor (PDGF)-AA and PDGF-CC were identified as major mediators that signal through PDGFR-alpha and thus induce HAS2-mediated HA synthesis in fibroblasts
Data suggest that the variant rs1425486 genotype could differentially affect targeting by miR-425 in ovarian cancer cells leading to higher PDGFC expression.
PDGFC mRNA expression were down-regulated in biopsies containing infiltrated lymphocytes or thyroiditis.
Upregulation of PDGFC expression may contribute to the clonal expansion of fibroid-derived smooth muscle cells in the development of uterine fibroids.
Data suggest that five novel genes, LUM, PDE3B, PDGF-C, NRG1 and PKD2, have great potential for predicting the efficacy of cisplatin-based chemotherapy against OSCC.
Results provide both in vitro and in vivo evidence that Mac-1 acting together with LRP1 facilitates PDGF-CC activation by thrombolytic tissue plasminogen activator in the neurovascular unit. The requirement of both Mac-1 and LRP1 for efficient activation of PDGF-CC by tPA provides a novel mechanism that helps limit PDGFRalpha signaling in the neurovascular unit.
PDGF-CC neutralization or deficiency was not associated with preservation or accelerated loss of peritubular capillaries, suggesting no significant pro-angiogenic effects of PDGF-CC during renal fibrosis
heme oxygenase-1 (HMOX1) activity is critically required for the vascular protective/survival effect of PDGF-CC.
Studied survival and antiapoptotic effects of PDGF-C on focal retinal lesions in Ccl2(-/-)/Cx3cr1(-/-) on C57BL/6N [Crb1(rd8)] (DKO rd8) background mice, a model for progressive and focal retinal degeneration.
loss of FREM1 function promotes epidermal blistering in Fraser syndrome as a consequence of reduced PDGFC activity, in addition to its stabilising role in the basement membrane
Study indicates the role for PDGF-C as a critical regulator of impaired angiogenesis of diabetes.
PDGF-C promotes tumor growth via a growth promoting effect on hepatic stellate cells that is dependent on the presence of functional PAK-2
Data identified PDGF-CC as an important candidate target gene for antiangiogenic therapy, and PDGF-CC inhibition may be of therapeutic value in treating neovascular diseases.
PDGF-CC is critically required for neuronal survival in both brain and retina. Its neuroprotective effect of PDGF-CC is achieved by regulating GSK3beta phosphorylation and expression.
During development, PDGF-C expression was widespread and dynamic, and found in somites and their derivatives, in kidney, lung, brain
Dominant negative PDGF-C inhibits growth of Ewing family tumor cell lines.
Data show that platelet-derived growth factor-C is a potent mitogen for cardiac fibroblasts, and overexpression results in an expansion of the interstitium that induces a secondary sex-dependent hypertrophic response in the cardiomyocytes.
role for PDGF-C in bleomycin-induced pulmonary fibrosis.
During mouse fetal development, PDGF C was expressed in the mesonephric mesenchyme, prefusion skeletal muscle, cardiac myoblasts, and in visceral and vascular smooth muscle.
Pdgfc(-/-) mice die in the perinatal period owing to feeding and respiratory difficulties associated with a complete cleft of the secondary palate.
PDGF-C is activated during lung development and is a potent growth factor for mesenchymal cells in vivo.
These results suggest that PDGF-C signaling is a new mechanism of cleft palate induced by RA.
The protein encoded by this gene is a member of the platelet-derived growth factor family. The four members of this family are mitogenic factors for cells of mesenchymal origin and are characterized by a core motif of eight cysteines. This gene product appears to form only homodimers. It differs from the platelet-derived growth factor alpha and beta polypeptides in having an unusual N-terminal domain, the CUB domain. Alternatively spliced transcript variants have been found for this gene.
platelet-derived growth factor C
, platelet-derived growth factor, C polypeptide
, spinal cord-derived growth factor
, secretory growth factor-like protein