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Validated All-in-One™ qPCR Primer for IL24(NM_006850.2) Search again
Product ID:
HQP001144
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
C49A, FISP, IL10B, MDA7, MOB5, ST16
Gene Description:
interleukin 24
Target Gene Accession:
NM_006850.2(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.
Validated result:
Summary
This gene encodes a member of the IL10 family of cytokines. It was identified as a gene induced during terminal differentiation in melanoma cells. The protein encoded by this gene can induce apoptosis selectively in various cancer cells.
Gene References into function
- these results provide compelling evidence for IL-24 being the fourth member of IL-10 family of cytokines to which their specific receptors have been identified.
- downregulation of expression in primary melanomas facilitates progression to invasive and metastatic stages
- Because blood leukocytes can be stimulated to produce MDA-7/IL-24, as well as respond to MDA-7/IL-24 by expressing secondary cytokines, MDA-7/IL-24 has the expression profile and major functional attributes that justify its designation as an interleukin.
- Inhibition of human lung cancer growth following adenovirus-mediated mda-7 gene expression in vivo.
- examination of ligand/receptor interactions and in signal transduction that may lead to specificity and distinct biology
- Review. mda-7 is a secreted protein with cytokine-like properties belonging to the IL-10 family. If delivered by an adenoviral vector, mda-7 induces selective apoptosis in cancer cells of diverse origin, while sparing their normal cellular counterparts.
- study demonstrate that expression of the MDA-7 tumor suppressor can negatively regulate iNOS expression in malignant melanoma cell lines
- Melanoma differentiation associated gene-7, mda-7/IL-24, selectively induces growth suppression, apoptosis and radiosensitization in malignant gliomas in a p53-independent manner.
- Signaling leading to susceptibility to MDA-7 induced apoptosis might be tyrosine kinase independent and can thus be distinguished from its cytokine function related properties mediated by IL-20/IL-22 receptor complexes requiring JAK/STAT kinase activity.
- in breast and lung tumor cells, MDA-7 protein expression modulates cell-cell adhesion and intracellular signaling via coordinate regulation of the beta-catenin and PI3K pathways
- Ad-mda7 exhibits selectivity in apoptosis induction and growth suppression in an atypical smooth muscle cell line
- Adenovirua-mediatd mda7 sensitizes NSCLC cells to ionizing radiation by suppressing the activity of NHEJ, a pathway essential for repair of radiation-induced DSBs.
- mda-7s expression is linked to a non-metastatic phenotype
- MDA-7/IL-24 has the ability to induce apoptosis in transformed cells, while having marginal growth suppressive effects on normal primary or immortalized cell lines.
- MDA-7 synergizes with tumor necrosis factor (TNF) for NF-kappa B activation and for NF-kappa B-mediated gene expression and can suppress the apoptotic effects of TNF.
- MDA-7 induces dose-dependent cell death in melanoma tumor cells
- Analysis of signal transduction changes in pancreatic carcinoma cells infected with Ad.mda-7 in combination with a ROS-inducer indicate that cell death correlates with modulation of discrete cassettes of multiple signaling pathways
- MDA-7/IL-24 status was a significant prognostic factor in lung adenocarcinoma, not in lung squamous cell carcinoma.
- identification of a novel bystander mechanism of MDA-7 killing in pancreatic cancer that functions via IL-20 receptors
- IL-24 is a member of IL-10 family of cytokines, and it signals through two hetorodimeric receptors, whose expression is also upregulated by ras oncogenes
- discriminating antitumor activity of MDA-7/IL-24 by presenting an unparalleled opportunity to develop improved therapeutic versions of this cancer-specific apoptosis-inducing cytokine.
- IL-19, IL-20 and IL-24 are distinct from classical ILs and constitute a separate subfamily of mediators within the IL-10 family
- IL-24 glycosylation is not mandatory for inducing cell death or bystander activities in different cancer cells.
- Establish MDA-7/IL-24 and GADD45alpha and GADD45gamma as critical mediators of apoptosis and growth arrest in response to NSAIDs in cancer cells.
- extended haplotype analysis revealed an association of IL19/IL20 haplotype GACACCGGAA with a higher risk for palmoplantar pustulosis (PPP) and of IL20/IL24 haplotype CAAAC with a reduced risk for PPP
- polymorphisms investigated are not associated with chronic periodontitis
- injection of adenovirus GFP/IL-24 significantly suppressed in vivo hepatocellular carcinoma growth in athymic nude mice
- MDA-7/IL-24 is ubiquitinated and degraded by the 26S proteasome
- These findings confirm that mda-7/IL-24 is a potent multidrug resistance (MDR) reversal agent, preferentially causing apoptosis in P-gp-overexpressing MDR cells.
- Both IL-20 and IL-24 showed correlations to CCL2/MCP-1 in plasma from rheumatoid arthritis and spondyloarthropathy patients.
- MDA-7/IL-24 has a role in inducing growth suppression and apoptosis of hepatoma
- GST-MDA-7 induces an endoplasmic reticulum stress response that is causal in the activation of multiple proapoptotic pathways.
- Regulation of GST-MDA-7 toxicity in human glioblastoma cells by ERBB1, ERK1/2, PI3K, and JNK1-3 pathway signaling.
- MDA-7/IL-24 plus radiation enhance survival in animals with intracranial primary human GBM tumors
- MDA7/IL-24 is the key cytokine to trigger the up-regulation of class I interferons.
- MDA-7/IL-24 protein induces stabilization of its own mRNA without activating its promoter. Furthermore, this posttranscriptional effect depends on de novo protein synthesis
- vectors targeting the ER (Ad-ER-mda7) may be more effective in cancer gene therapy possibly through more effective induction or ER stress pathways
- Adenovirus vector expressing mda-7 selectively kills hepatocellular carcinoma cell line Hep3B.
- The addition of recombinant IL-24 to IL-2-activated chronic lymphocytic leukemia B cells results in increases of transcription, protein synthesis. and phosphorylation of p53.
- IL-24 overcomes temozolomide resistance and enhances cell death by down-regulation of O6-methylguanine-DNA methyltransferase in human melanoma cells
