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Validated All-in-One™ qPCR Primer for IFNA1(NM_024013.2) Search again
Product ID:
HQP067206
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
IFL, IFN, IFN-ALPHA, IFN-alphaD, IFNA13, IFNA@, leIF D
Gene Description:
interferon alpha 1
Target Gene Accession:
NM_024013.2(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.
Summary
Leukocyte interferon is produced predominantly by B lymphocytes. Immune interferon (IFN-gamma; MIM 147570) is produced by mitogen- or antigen-stimulated T lymphocytes.[supplied by OMIM].
Gene References into function
- Alpha interferon suppresses the cyclin D3 and cdc25A genes, leading to a reversible G0-like arrest.
- Results show that a significant positive relationship exists between IFNalpha production capacity and the clinicopathological parameters of deteriorated renal lesions in the acute but not in the latent phase of IGA nephropathy.
- Production of matrix metalloproteinase-9 in early stage B-CLL is suppressed by interferons alpha and gamma.
- Endogenous interferon-alpha production by differentiating human monocytes regulates expression and function of the IL-2/IL-4 receptor gamma chain
- Interferon-alpha (Intron A) upregulates urokinase-type plasminogen activator receptor gene expression
- Response of hairy cells to IFN-alpha involves induction of apoptosis through autocrine TNF-alpha and protection by adhesive proteins (vitronectin).
- IFN-alpha up-regulates APO2L-mediated lysis of a CD4+ cytotoxic T lymphocyte clone against its autologous tumor in vitro and in vivo.
- whereas viruses trigger cells to produce IFN-I, the amount of IFN is tightly controlled by cytokines
- demonstrated that IFN-alpha activates STAT4 directly and that this is required for IFN-gamma production during viral infections in concert with T cell receptor-derived signals
- Human IFN-alpha may enhance biological defense activities against oxidative stress and function as a potent fibrosuppressant by protecting rat hepatocytes and hepatic stellate cells from lipid peroxidation in vivo.
- Interferon-alpha induces expression of myeloblastin and a specific T-cell response in chronic myeloid leukemia
- Circulating, interferon alpha-producing plasmacytoid dendritic cells decline during human ageing.
- High levels of serum IFN-alpha are correlated with febrile seizures in influenza.
- IFN-alpha is secreted by fungi-prestimulated leukocytes from the lower respiratory tract and may be involved in the processes of exacerbation of asthma complicated by fungal infections
- IFN-alpha stimulates induction of MICA/MICB on dendritic cells, a mechanism by which NK cells are activated.
- MHC Class II proteins, interferon-alpha, interferon-gamma receptor and the capacity to present antigen may be crucial in HIV-associated nephropathy pathogenesis.
- primarily mediates effects on megakaryocytic cells and platelets rather than on thrombopoietin-producing hepatocytes
- expression modulated by co expression of hepatitis C virus NS5A protein and human homeodomain protein PTX1
- IFN-alpha alone is able to induce the secretion of small amounts of IP-10 in plasmacytoid dendritic cells and is found to synergize with low concentrations of IFN-gamma, in a Th1-like environment.
- IFN-alpha and ribavirin being taken in a combination drug therapy for chronic hepatits C had no adverse fetal effects.
- Measles virus V protein blocks IFN-alpha by inhibiting STAT1 and STAT2 phosphorylation.
- IFN-alpha recruits both IFN regulatory factor 1 and Stat3 transcription factors to the human IL-10 promoter.
- NK cells displayed apparently augmented cytotoxicity against target tumor cells (K562) and up-regulated gene expression of cytolytic effectors Fas-L and perforin in response to IFNalpha stimulation
- Peripheral blood monocytes cultured in the presence of IFN-alpha can differentiate into dendritic cells (DCs) expressing a number of Toll-like receptors (TLRs), including TLR7, which is classically found on natural type I IFN-producing plasmacytoid DCs.
- IFN-alpha is a relevant in vivo regulator of CD73 (ecto-5'-nucleotidase) in the endothelial-leukocyte microenvironment in infections and thus has a fundamental role in controlling the extent of inflammation via CD73-dependent adenosine production.
- an intact PI3K/mTOR pathway is necessary for the ability of IFNalpha to induce apoptosis, whereas activation of the Jak-STAT pathway alone appears to be insufficient for this specific IFNalpha-induced effect
- Interferon alpha but not interleukin 12 activates STAT4 signaling in human vascular endothelial cells
- The IFN alpha inducers probably consist of immune complexes (ICs) containing RNA and possibly DNA as essential interferogenic components in systemic lupus erythematosus
- Our results demonstrate that SOCS-1 and SOCS-3 proteins inhibit IFN-alpha-induced activation of the Jak-STAT pathway and expression of the antiviral proteins 2',5'-OAS and MxA.
- thymidine phosphorylase mRNA and activity expression is upregulated 2-3 fold after treatment with interferon alpha
- Thymic plasmacytoid dendritic cells (pDC)modulate HIV-1 replication through secretion of IFN-alpha. The degree of inhibition depends on the level of IFN-alpha produced by the thymic pDC.
- type I interferons interact with receptor components results and have roles in the activation of a number of signaling pathways [review]
- In testing the contribution of IFN-alpha secreted during infection with Mycobacterium tuberculosis to inhibition of signaling, it is found that it is necessary, but not sufficient.
- no IFN-alpha genotype was significantly associated with the risk of SLE.
- IFN-alpha sensitizes cells to microbial recognition by up-regulating the expression of several Toll-like receptors (TLRs) as well as adapter molecules and kinases involved in TLR signaling.
- interferon alpha has a role in regulating the p70 S6 kinase pathway in chronic myelogenous leukemia cells
- Demdritic cells express and store IFN-alpha in to confer resistance to foot and mouth disase virus.
- In the IFN signaling pathway leading to STAT activation, both JAK1 and TYK2 are essential, whereas NF-kappaB activation requires only TYK2.
- NKp44 is present on a subset of natural interferon-producing cells (IPCs) in tonsils. Crosslinking of NKp44 does not trigger IPC-mediated cytotoxicity but, paradoxically, inhibits IFN-alpha production by IPCs in response to CpG oligonucleotides.
- Taken together, IFN-alpha-induced activations of NF-kappaB and COX-2 were inhibited by the addition of curcumin in A549 cells.
- Investigation of the mechanism of HCV action on IFN-alpha showed that IRF-7-induced IFN-alpha promoter activation was inhibited in the HCV replicon cells
- Our results suggest that IFN-alpha and TNF-alpha have a significant role in priming epithelial cells for higher cytokine and chemokine production in influenza A virus infection.
- APOBEC3G is induced by IFN stimulation in human hepatocytes and thus could be involved in host defense mechanisms directed against hepatitis viruses
- IFN-alpha exhibits readily detectable, high-affinity interactions with human complement receptor 2.
- results show that in epithelial cells influenza A virus-induced antiviral cytokine gene expression is triggered by RIG-I and mda-5, whose expression is positively regulated by IFN-alpha.
- Reduced endogenous levels of the potent antiviral agent IFN-alpha may interfere with T cell-mediated immune responses leading to increased susceptibility and persistence of infections in persons with diabetes.
- Data describe the species specificity of IFN-alphas, the residues in murine IFN-alpha4 that preclude strong affinity interactions with human IFNAR1 and 2, and residues in human IFN-alpha8 that resemble a receptor interactive domain in murine IFN-alpha4.
- In short term blast lines from patients with AML, additive effects of IFN-alpha and LPS on Caspase-8 dependent apoptosis was observed only with few samples
- Experience with oral interferon-alpha in patients with thrombocytosis and polycythemia vera is reported.
- IFN-alpha fails to promote T helper cell type 1 commitment in human CD4+ T cells because of attenuated STAT4 phosphorylation, which was insufficient to induce stable expression of transcription factor T-bet.
- Addition of interferon alpha to monocyte-derived dendritic cells or pretreatment with Toll-like receptor ligands protects against infection and the cytopathic effects of avian influenza H5N1 virus.
- The induction of IFIT4 transcription by IFN-alpha depends upon sequential activation of PKCdelta, JNK and STAT1, and the influence of PKCdelta or JNK on IFN-alpha-mediated induction of IFIT4 is dependent upon the phosphorylation of STAT1 at Ser-727.
- IFN-alpha produced after HIV-induced Toll-like receptor 7 stimulation was responsible for TRAIL expression and the down-regulation of both CXCR4 and CCR5 by IKpDC
- depletion of endothelial progenitor cells caused by excessive IFN-I may be linked to endothelial dysfunction and increased cardiovascular risk in systemic lupus erythematosus
- Dermatomyositis and polymyositis are diseases characterized by the systemic overexpression of IFNalpha/beta-inducible genes
- IFNalpha activity and BAFF levels are elevated in the plasma of patients with Sjogren's syndrome compared with healthy controls.
- Activation of interfeon-alpha pathways up-regulates Ro52 at the mRNA level and leads to translocation of the Ro52 protein (E3 ligase) from cytoplasm to cell nucleus.
- impairment of IFN-alpha production may be linked to an increased cancer risk and dysfunction of the IFN system is associated with cancer. Assessment of IFN-alpha production can be a potential test for the early detection of cancer in humans.
- Data demonstrate that human metapneumovirus can inhibit the interferon-alpha response through regulation of STAT1 phosphorylation, and provide important insight into the viral pathogenesis of hMPV infection in the respiratory tract.
- Our data indicate that plasmacytoid dendritic cells are protected by an IFN-alpha mediated upregulation of APOBEC3G type of innate immunity from HIV-1 infection.
- Flowcytometric analyses revealed that incubation of CD14+ monocytes with IFNalpha results in a steady increase of CD56 surface expression of these cells.
- Blockade of Treg cell-mediated suppression by IFNalpha-producing antigen-presenting cells in systemic lupus erythematosus patients may contribute to a pathogenic loss of peripheral tolerance in this disease.
- plasmacytoid dendritic cells (pDCs) from allergic subjects produced sixfold less IFN-alpha when stimulated with CpG .
- DC-SIGN enhances the production of IFN-alpha and TNF-alpha in cells that infected by glycosylated West Nile virus.
- higher INFalpha activity at younger age in SLE patients supports a primary pathogenic role of IFNALPHA in SLE
- study concludes that IFN-alpha induces the transcription of HIF-1alpha in human endothelial cells though a JAK-ISGF3 pathway under normoxic conditions, and that this response contributes to the antiproliferative activity of this cytokine
- ISRE, STAT1, and STAT2 have essential roles in the regulation of constitutive and IFN-alpha-mediated PD-1 expression in macrophages
- IFNalpha down-regulates IL-17 expression and Th17 differentiation in vitro and in vivo.
- IFN-alpha synergizes with interleukin (IL)-12 in regulating the development of IL-2-secreting human T(central memory) cells.
- Significantly higher interferogenic activity is found in cerebrospinal fluid, but not the serum, of patients with neuropsychiatric lupus erythematosus.
