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Validated All-in-One™ qPCR Primer for CD274(NM_014143.3) Search again
Product ID:
HQP099747
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1, PDL1, hPD-L1
Gene Description:
CD274 molecule
Target Gene Accession:
NM_014143.3(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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- Cancer cell-associated B7-H1 increases apoptosis of antigen-specific human T-cell clones in vitro
- B7-H1 is inducible on human endothelial cells by IFN-gamma both in vitro and in vivo; blocking its interaction with its receptor (PD-1) on T cells augments T cell cytokine synthesis.
- up-regulation in HIV infection, relation to disease progression, and possible role in AIDS progression
- Blockade of PD-L1 during T cell responses initiated by allogenic dendritic cells increases T cell proliferation and cytokine production, showing that PD-L1 functions to inhibit T cell activation.
- Monoclonal antibody DF272-defined surface molecule B7-H1 represents a unique receptor structure on dendritic cells that may play a role in the induction and maintenance of T cell anergy.
- binding properties of B7-H1 to programmed death-1.
- B7-H1 is expressed in muscle cells and may have a negative immune regulatory function in idiopathic inflammatory myopathies.
- review of the negative immunoregulatory role of B7-H1 documented in human diseases, including cancer and auotimmune diseases
- Inflammatory bowel disease intestinal epithelial cell (IEC) surface expressed B7h and B7-H1. Proliferation of IEC-stimulated T cells was inhibited only by B7h immunoglobulin. Interferon gamma was inhibited by both anti-B7h mAb and B7h Ig.
- B7-H1 may have a role in antitumor immune responses in non-small cell lung cancer
- IFN-beta up-regulates B7-H1 in vitro and in MS patients in vivo and might represent a novel mechanism how IFN-beta acts as a negative modulator on APC T-cell interactions in the periphery.
- Data suggest that PD-L1 status may be a new predictor of prognosis for patients with esophageal cancer.
- B7 homolog 1 (B7H1) may be involved in the immune evasion of human glioma
- Inhibitory signals delivered from human rhinovirus HRV14-treated dendritic cells to T cells via B7-H1 are critical for induction of T-cell anergy.
- dermal fibroblasts express the B7-H1 mRNA in the process of skin inflammation, suggesting the involvement of NF-kappaB and MAPK and PI3K
- Interaction of tubular epithelial cells and kidney infiltrating T cells via ICOS-L and B7-H1 may change the balance of positive and negative signals to the T cells
- dysfunction of the PD-1/PD-L1 pathway may be related to tolerance for lymphocytes, which causes Sjogren syndrome
- B7-H1 is inducible renal tubular epithelial antigen that inhibits T cell activation. B7-H1/PD-1 pathway might play role in protecting tubular epithelium from immune-mediated damage. B7-H1 may be therapeutic strategy in autoimmune renal diseases.
- Our data suggest that PD-L1/PD-1 interactions negatively regulate T cell effector functions predominantly in the absence of exogenous cytokine support, indicating an important role for this pathway in tumor evasion.
- B7-H1 is involved in suppression of T cell proliferation and IL-2 synthesis, roles suggested for B7-H1 on the gastric epithelium that contribute to the chronicity of Helicobacter pylori infection.
- Multivariate analysis demonstrated that PD-L1 immunodetection could be used as an independent factor to evaluate the prognosis of gastric carcinoma.
- a novel bidirectional interaction between hepatocytes and lymphocytes modulated by PD-L1 expression in hepatocytes may contribute to the unique immunological properties of the liver
- Overexpression reduces accessory immune functions of endothelial cells.
- data do not support an association between systemic lupus erythematosus and SNP's within the genes of the PDCD1 ligands PD-L1 and PD-L2
- The aberrant expression of B7-H1 in urothelial cancer is associated with aggressive tumors, suggesting a regulatory role of tumor-associated B7-H1 in antitumor immunity.
- Modulation of PD-L1 system may play a role in the development of autoimmune liver diseases.
- Programmed cell death 1 ligand 1 and tumor-infiltrating CD8+ T lymphocytes are prognostic factors of human ovarian cancer.
- Inhibition of the MyD88 and TRAF6 adaptor proteins of the TLR pathway blocked not only B7-H1 expression induced by TLR ligands but also that mediated by IFN-gamma
- B7-H1 was downregulated in quiescent cells and upregulated in cells stimulated with a mitogen confirming the association of proliferation with the induction of B7-H1.
- Elevated B7-H1 expression is closely associated with the suppression of T cell immune function in chronic hepatitis B patients.
- Induction of cells of the T regulatory (Treg) phenotype by B7-H1 may play an important role in the T-cell suppression associated with Helicobacter pylori infection, as well as other infections that result in an up-regulation of B7-H1.
- PD-L1 polymorphisms are not associated with susceptibility to rheumatoid arthritis, but 6777 G is associated with the prevalence of rheumatoid nodule in Taiwanese patients.
- results indicate Hepatitis C virus core can upregulate a key negative T cell signaling pathway, PD-1/PDL-1, associated with viral persistence & expressed on T cells of infected individuals
- chemopreventive agents were able to induce PD-L1 surface expression in human breast cancer cells, which then promoted PD-L1-mediated T cell apoptosis, a potential link between chemotherapy and cancer immunoresistance
- PD-L1-deficient transgenic mice reconstituted with bone marrow from wild-type mice remain susceptible to severe myocarditis, demonstrating the protective effect of PD-L1 on non-bone marrow-derived cells.
- results suggest that the PD-1/PD-L1 pathway may play a regulatory role in memory T cell subsets in addition to its association with T-cell exhaustion
- Blockade of the B7-H1 pathway may represent an attractive approach in the treatment of chronic hepatitis C.
- Induction and maintenance of T cell tolerance requires PD-1, and its ligand PD-L1 on nonhematopoietic cells can limit effector T cell responses and protect tissues from immune-mediated tissue damage.
- deficient cellular immunity observed in Hodgkin lymphoma patients can be explained by "T-cell exhaustion," which is led by the activation of PD-1-PD-L signaling pathway
- B7-H1, PD-1 and FOXP3 may have roles in progression of breast neoplasms
- possible functional relationship between the enhanced incidence of precursor plasmacytoid dendritic cells, their comparatively high relative expression of the coinhibitory molecule PD-L1
- PD-L1 polymorphism plays a role in Graves' disease (GD) development, and GD patients with the C allele at position 8923 in PD-L1 gene had difficulty in achieving remission.
- up-regulated B7-H1 expression in human pancreatic carcinoma tissues, which might play a role in tumor progression and invasiveness.
- HRV-16 infection or exposure to dsRNA induces epithelial B7-H1 and B7-DC.
- data provide evidence that neurons can express the B7-H1 molecule after viral stress or exposure to a particular cytokine environment
- Hepatitis c virus-specific CD8 T-cell dysfunction and responsiveness to PD-1/PD-L blockade are defined by their PD-1 expression and compartmentalization.
- The PDCD1:CD274 pathway functions in modification of maternal decidual lymphocyte cytokine secretion during pregnancy.
- PD-1 has a key regulatory role during the immune response of the host to the pathogen
- Triptolide inhibits interferon-gamma-induced programmed death-1-ligand 1 surface expression in breast cancer cells.
- PD-L1 may play an important and undervalued role on human T cells.
- Activation of TLR4 signaling in bladder cancer cells up-regulated B7-H1 expression. This regulation was significantly attenuated by ERK or JNK inhibitor.
- findings show monocytes & CCR5(+) T cells of HIV-uninfected donors upregulate PDL-1 on in vitro exposure to HIV; HIV-induced PDL-1 required interferon alpha; in setting of HIV infection, IFN-alpha may negatively affect T cell responses by inducing PDL-1
- B7-H3 is highly expressed in urothelial cell carcinoma across tumor stages, whereas B7-H1 and PD-1 expression are associated with advanced disease
- PD-L1 expression is central to autoimmune heart and lung disease in lupus-susceptible (MRL) mice, since PD-L1-null MRL mice succumb to autoimmune myocarditis and pneumonitis before developing renal or systemic illness.
- B7-H1 is highly expressed on leukemia cells of acute monocyte leukemia (M5) patients
- stromal myofibroblasts and fibroblasts may limit T-helper cell proliferative activity in the gut and, thus, might play a prominent role in mucosal intestinal tolerance via PD-L1
- PD-1/PD-L1 expression on cells from asymptomatic HTLV-1 carriers and ATLL patients in comparison with cells from healthy donors.
- B7-H1 inhibitory signaling may reversely mediate functional impairment of mDC in HIV-1 infection, which further supports the notion that B7-H1 blockade represents a novel therapeutic approach to this disease.
- B7-H1 stimulation activates phosphorylation of JNK and c-jun and down-regulates mitogen-activated protein kinases 1/2 and akt proto-oncogene protein.
- PD-1/PD-L1 interaction is essential for the induction and maintenance of Invariant NKT cell anergy.
- These results highlight a novel mechanism for regulation of B7 family proteins in the placenta.
- B7-H1 gene transcription and protein synthesis was enhanced by C5b-9.
- Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1).(
- The expression of PD-1/PDL-1 in renal tissue and during mixed lymphocyte reactions suggests an important role in regulating peripheral T cell tolerance