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Validated All-in-One™ qPCR Primer for SPARC(NM_003118.3) Search again
Product ID:
HQP055553
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
BM-40, OI17, ON, ONT
Gene Description:
secreted protein acidic and cysteine rich
Target Gene Accession:
NM_003118.3(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:
Summary
Secreted protein acidic and rich in cysteine/osteonectin/BM40, or SPARC, is a matrix-associated protein that elicits changes in cell shape, inhibits cell-cycle progression, and influences the synthesis of extracellular matrix (ECM) (Bradshaw et al., 2003 [PubMed 12721366]).[supplied by OMIM].
Gene References into function
- SPARC is induced by VEGF and plays a dual role in the VEGF functions, tumor angiogenesis, and extravasation of tumors mediated by the increased permeability of endothelial barrier function.
- SPARC modulates cell growth, attachment and migration of U87 glioma cells on brain extracellular matrix proteins.
- Osteonectin/SPARC induction by ectopic beta(3) integrin in human radial growth phase primary melanoma cells.
- osteonectin was present mostly in the nonmineralized predentin.
- MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmoary fibrosis
- may have role in remodeling and repair of periodontal tissue by promoting proliferation and matrix metalloproteinase-2 production; may regulate osteoclast formation through osteoprotegerin/osteoclastogenesis inhibitory factor in periodontal ligament cell
- SPARC plays an important role in stimulating motility and the invasive behavior of c-Jun/MCF7 cells and that SPARC promoter activation by c-Jun appears to occur through an indirect mechanism.
- Quantitative analysis of osteonectin mRNA in thyroid carcinomas. Increased expression of osteonectin mRNA was observed in anaplastic carcinoma tissue.
- These studies co-localize SPARC to several sites of renal injury previously shown to be sites of PDGF B-chain expression and/or activity.
- the migration of retinal pigment cells in epiretinal membranes is modulated by TSP1 and SPARC and thus that these two proteins ultimately may represent therapeutic targets in the management of the membranes.
- proteolysis of SPARC by MMP-3 produced peptides that regulate endothelial cell proliferation and influence angiogenesis
- In NSCLC, SPARC is selectively synthesized by the cells of the tumoral stroma.
- High SPARC expression showed a trend toward longer survival in non-small cell lung cancer.
- Increased osteonecrin expression is associated with malignant cell transformation of the lung.
- New insights into matricellular trafficking of SPARC. Intra- and extra-cellular localization patterns may influence development, homeostasis, and differentiation of transitional epithelium.
- SPARC expression increases glioma cell survival under stress initiated by serum withdrawal through a decrease in apoptosis.
- SPARC was measured in discs of subjects aged 0-76 years. SPARC may have an unrecognized role in disc remodeling, aging, and degeneration.
- Overexpression of SPARC gene is associated with human gastric carcinoma
- TGFbeta1 can induce increased expression of both SPARC and type I collagen. Specific inhibition of SPARC led to decreased expression of type I collagen and attenuated the profibrotic effect of TGFbeta1 in cultured normal human fibroblasts.
- loss of expression of SPARC gene and promoter methylation in lung cancers
- SPARC plays a crucial role in tumour development in breast cancer
- gamma linolenic acid is a regulator of SPARC secretion and expression in cancer cells
- expression of SPARC in fibroblasts and endothelial cells derived from young donors and old donors decreased 1.6 to 2.3-fold with age
- it was concluded that secreted protein acid rich in cysteine(SPARC) overexpression is a constant and functionally important feature of invasive ductal carcinomas of the breast
- Results show that SPARC can be a beneficial prognostic marker for the stage II tongue carcinoma, of which clinical outcomes are sometimes difficult to predict.
- Data suggest that the motif of SPARC responsible for anti-spreading activity is dependent on the coordination of calcium by a glutamate residue at the Z position of EF-hand 2.
- We concluded that osteonectin was not a chemotactic factor. However, through its anti-adhesive properties, osteonectin induced undirected breast cancer cell motility, and may have enhanced chemoattraction to vitronectin.
- Data show that SPARC binds to plasmin-cleaved fibrinogen, but not to native fibrinogen.
- SPARC or its combination with glypican-3 is considered a potentially useful tumor marker, especially for melanoma at an early stage.
- Clearance of SPARC from the extracellular space by alternatively activated macrophages regulates tissue remodeling and extracellular matrix synthesis.
- Results suggest a possible role for secreted protein, acidic, cysteine-rich (SPARC) in development of functional and/or structural zonation of the human fetal adrenal
- destruction of the basement membrane and appearance of SPARC+ spindle cells are not coincident during the course of brain invasion by meningiomas
- High levels of SPARC are not required for tumor progression, but are necessary for tumor growth and maintenance.
- data further demonstrate the role of SPARC in glioma tumor progression through the activation of intracellular kinases that may provide novel therapeutic targets for advanced cancers
- The expression of SPARC by peritumoral fibroblasts portends a poorer prognosis for patients with pancreatic cancer
- Results show for the first time that forced-expression of SATB1 in K562 cells triggers SPARC up-regulation by binding to a 17bp DNA sequence in the third intron.
- The results indicate that epigenetic gene silencing of SPARC is frequent in colon cancers, and that inactivation of SPARC is related to rapid progression of colon cancers.
- A negative association is noted for alveolar bone loss and salivary osteonectin in postmenopausal women.
- Accumulation of SPARC protein in most tumors compared to normal tissues (p<0.025), suggests an important role in the carcinogenesis of endometrial tumors.
- Our results suggest that their upregulation and activation may be a consequence of increased SPARC expression. These data provide a provisional mechanism whereby SPARC contributes to brain tumor invasion.
- The motif of SPARC that inhibits the synthesis of urothelial cell DNA is not a nuclear localization signal
- Melanoma growth is not subject to regulation by exogenous SPARC, nor by stromal organization, but only by SPARC levels produced by the malignant cells themselves.
- p45-sErbB3 may mediate the bidirectional interactions between prostate cancer cells and bone via osteonectin
- Therapeutic targeting of SPARC in nasopharyngeal angiofibroma would be targeting of a molecule at the roots of cooperation between stromatogenesis and angiogenesis
- Central role for Osteonectin in the regulation of gene expression changes driving the progression of melanoma toward metastasis.
- No association between SPARC gene polymorphism and gingival overgrowth was revealed in kidney transplant patients who were administered CsA.
- Transient re-expression of SPARC in SPARC-downregulated melanoma cells reverted extracellular N-CAD, CLU, and HSP27 to levels similar to those in the control.
- Malignant cells expressing or not expressing SPARC developed alternative mechanisms that, in contrary to stromal cells, rendered them SPARC-insensitive. Overexpression of SPARC by melanoma cells renders them resistant to the effect of exogenous SPARC.
- Osteonectin regulates skeletal remodeling and bone mass in animals, and haplotypes in the 3' UTR of this gene are associated with bone density in Caucasian men with idiopathic osteoporosis.
- analysis of the role of SPARC in tumor progression [review]
- experiments implicate a novel mechanism, whereby SPARC regulates VEGF function by limiting the available growth factor
- Data show that the nonsteroidal anti-inflammatory drug NS398 reactivates SPARC expression via promoter demethylation to attenuate invasiveness of lung cancer cells.
- could play a crucial role in dental pulp tissue repair by inducing dental pulp cell migration via extracellular signal-regulated kinase
- SPARC subcellular localization in the human osteoblastic HOBIT cell line was investigated by immunocytochemistry and western blot analysis.
- Expression of SPARC is associated with elongated cell morphology, and increased migration and invasion.
- SPARC might modulate collagen fibril assembly in vivo.
- SPARC-mediated mobilization of adipose stromal (stem) cells through its effect on alpha5beta1 integrin complex provides a functional basis for the regulation of white adipose tissue body composition by SPARC.
- This study shows SPARC expression both during muscle development and in regenerating muscle. The expression is detected both in satellite cells/myoblasts and in myotubes and muscle fibers, indicating a role for SPARC in the skeletal muscle compartment.
- The effects of tumor SPARC as a negative regulator of ovarian cancer are mediated through decreased recruitment of macrophages and downregulation of the associated inflammation.
- SPARC expression appears to be closely related to malignancy in melanocytic lesions.
- SPARC was significantly increased in the primary angle closure glaucoma iris.
