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Validated All-in-One™ qPCR Primer for PTN(NM_002825.6) Search again
Product ID:
HQP015778
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
HARP, HB-GAM, HBBM, HBGF-8, HBGF8, HBNF, HBNF-1, NEGF1, OSF-1
Gene Description:
pleiotrophin
Target Gene Accession:
NM_002825.6(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- Pleiotrophin signaling through anaplastic lymphoma kinase is rate-limiting for glioblastoma growth.
- overexpression of Pleiotrophin is associated with inflammation and pancreatic cancer
- induced the stimulation of tritiated thymidine incorporation in quiescent human peripheral blood mononuclear cells in a dose-dependant manner
- PTN induces weak chemotactic and strong haptotactic migration of glioblastoma and cerebral microvascular endothelial cells.
- In the present study, we demonstrate that HARP is secreted in human mature milk with concentrations ranging from 17.68+/-6.4ng/ml in mature milk to 59.9+/-11.22ng/ml in colostrum.
- angiogenic factor HARP can also negatively regulate the angiogenic activity of VEGF165
- in the OSF1 transgenic line, bone mass increase was evident in female, but not male, mice [OSF1]
- Results describe the influence of mechanical loading on heparin binding growth associated molecule (HB-GAM) expression in bone cells.
- Heparin-binding growth-associated molecule is overexpressed in malignant glioma cells and is involved in tumor growth.
- RPTPbeta/zeta is a receptor of HARP in human endothelial cells
- JUN-dependent expression of PTN and SDF-1 in fibroblasts has a role in keratinocyte proliferation
- report on the presence and purification of two naturally occurring forms of PTN (18 and 15 kDa) that differentially promote glioblastoma migration and proliferation
- HARP seems to act as an important regulator of diverse biological activities in human prostate cancer cells
- PTN signals new blood vessel formation through its ability to stimulate different functions in different cell types not limited to the endothelial cell
- conclude that pleiotrophin(PTN) is a rate-limiting growth factor in glioblastoma
- results demonstrate that PTN inhibits HIV infection and suggest that the cell surface-expressed nucleolin is a low affinity receptor for PTN binding to cells and it is also implicated in PTN entry into cells by an active process
- results show that heparin affin regulatory peptide (HARP) is important for human prostate cancer cell proliferation and migration and establish role of activator protein-1 in up-regulation of HARP expression by low concentrations of hydrogen peroxide
- the binding of pleiotrophin to chondroitin sulfate is regulated by chain length and oversulfated structures
- The data demonstrated that the extracellular signal-regulated kinase (ERK) 1/2 pathway, PKC, PKA, p38, and c-Jun N-terminal kinase MAPK participated in the mechanical downregulation of HB-GAM expression.
- HARP mediates FGF2 stimulatory effects on prostate cancer cells.
- This is the first description of the expression of PTN by human MCs and the data suggest that it is rapidly induced in cells that are triggered to migrate.
- PTN signaling may have a critical role in chromosomal segregation and cell cycle progression.
- Data suggest that increased tyrosine phosphorylation of receptor protein tyrosine phosphatase beta/zeta substrates in pleiotrophin-stimulated cells is sufficient to coordinately stimulate the functions needed for an epithelial-mesenchymal transition.
- Pleiotrophin is a neurotrophic factor for spinal motor neurons
- PTN was identified as a factor that plays a role in the nigrostriatal system during development and in response to disease, and may therefore be useful for neuroprotection or reconstruction of the dopamine
- Inhibition of PTN with a polyclonal anti-PTN antibody reduced growth and enhanced apoptosis of MM cell lines and freshly isolated bone marrow tumor cells from MM patients
- PTN expression is associated with histopathological grade of astrocytomas
- Pleiotrophin is present in pathologic human intervertebral discs, and its prevalence and distribution suggest that it may play a role in neovascularization of diseased or damaged disc tissue
- secretion of PTN through stimulation of the stromal cell microenvironment alone may be sufficient to account for significant features of breast cancer progression.
- Inhibition of the mitogenic, angiogenic, and tumorigenic activities of PTN by a synthetic peptide corresponding to its C-thrombospondin repeat-I domain.
- phosphorylation of ALK in PTN-stimulated cells is mediated through the PTN/RPTPbeta/zeta signaling pathway
- identified the exact molecular domain involved in inhibition of HARP-induced mitogenesis
- An autologous PTN-pleiotrophin receptor (PTPRZ1) signaling loop is present in human embryonic stem cells and functions here predominantly via an antiapoptotic effect.
- HARP negatively affects diverse biological activities in C6 glioma cells, mainly due to binding of HARP to VEGF, which may sequester secreted VEGF from signalling through VEGFR2.
- Pleiotrophin failed to activate anaplastic lymphoma kinase (ALK) in neuroblastoma/glioblastoma cells expressing this receptor. ALK is still an orphan receptor in vertebrates.
- MMP-2 processing of HARP and CTGF released vascular endothelial growth factor (VEGF) from angiogenic inhibitory complexes.
- pleiotrophin potentiates cardiomyocyte cell death, at least partially, through inhibition of AKT signaling
- PTN was expressed in HSCs, Kupffer cells, and hepatocytes in fibrotic liver. We propose that pleitrophin specifically antagonizes the TGFbeta1 activity during liver fibrosis
- pleiotrophin (PTN) and syndecan-2 and -3 as direct binding partners of Y-P30.
- PTN through its receptor RPTPbeta/zeta is a mediator of the stimulatory effects of eNOS/NO on human endothelial and prostate cancer cell migration
