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Validated All-in-One™ qPCR Primer for GDF15(NM_004864.3) Search again
Product ID:
HQP116757
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GDF-15, MIC-1, MIC1, NAG-1, PDF, PLAB, PTGFB
Gene Description:
growth differentiation factor 15
Target Gene Accession:
NM_004864.3(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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Summary
Bone morphogenetic proteins (e.g., BMP5; MIM 112265) are members of the transforming growth factor-beta (see TGFB1; MIM 190180) superfamily and regulate tissue differentiation and maintenance. They are synthesized as precursor molecules that are processed at a dibasic cleavage site to release C-terminal domains containing a characteristic motif of 7 conserved cysteines in the mature protein.[supplied by OMIM].
Gene References into function
- MIC-1, a divergent TGF-b superfamily cytokine, was cloned from a U937 subtracted cDNA library enriched for activation-associated sequences. It is induced in macrophages by many activation-associated stimuli but not LPS or IFN-g
- Unlike other TGF-b cytokines, MIC-1 is able to be expressed correctly folded without its propeptide. A 28 aa propeptide epitope contains a quality control signal which can signal misfolding of MIC-1, leading to proteasomal degradation.
- MIC-1 is present in large amounts in placenta and amniotic fluid. Very high levels of MIC-1 are present in the sera of pregnant women and rise substantially with progress of gestation
- At least five immunogenic regions on the MIC-1 surface can be detected by MAbs. One MAb is directed against the amino terminus of the protein and can distinguish between the two allelic forms of MIC-1
- NAG-1 is an antitumorigenic and proapoptotic protein, and its regulation by COX inhibitors may provide new clues for explaining their proapoptotic and antitumorigenic activities.
- Propeptide deletion mutants of MIC-1 enabled identification of a region between residues 56 and 78, which is important for the interaction between the propeptide and the mature peptide during folding
- the level of expression of the NAG-1 gene will depend on the availability of Sp proteins and on co-factors such as chicken ovalbumin upstream promoter-transcription factor 1
- Resveratrol enhances the expression of non-steroidal anti-inflammatory drug-activated gene (NAG-1) by increasing the expression of p53
- report that autocrine hGH production by mammary carcinoma cells specifically results in the transcriptional repression of the p53-regulated placental transforming growth factor-beta gene (Placental growth factor-beta; TGF-beta)
- placental transforming growth factor-beta as an important downstream mediator of DNA damage signaling and a transcriptional target of p53 (PTGF-beta)
- Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1. MIC-1 is an important downstream mediator of p53 function and intercessor of cellular stress signaling and exerting antitumorigenic activities.
- In the experimental model MIC-1 may exert anti-tumorigenic properties via a paracrine mechanism mediated by host cells in vivo. MIC-1 is an important downstream mediator of p53 function
- MIC-1 serum levels were higher at baseline in women who later had cardiovascular events. Levels > 90th percentile were associated with a 2.7x greater risk and independent of traditional cardiovascular risk factors and at least additive to that of CRP
- There are at least two alleles of MIC-1 that are due to a G-->C point substitution at position 6 of the mature protein, which alters a his to an asp (MIC-1 H and MIC-1 D). The frequency of the 3 common MIC-1 genotypes was: HH 54%; HD 39%; DD 7%
- GDF-15 prevents apoptosis in cerebellar granule neurons by activating Akt and inhibiting endogenously active ERK
- Microarray analysis identifies MIC-1 as being upregulated in cancer of breast, prostate, and colon. Tissues from these patients show increased MIC-1 by IHC and their serum shows elevated levels
- There is a strong association between MIC-1 serum levels and neoplastic progression (polyps to cancer) within the large bowel and significant differences in time to relapse and overall survival between subjects with different MIC-1 levels and genotypes
- Decreased NAG-1 expression in higher grade cancer is consistent with its known antitumorigenic, proapoptotic activities.
- amniotic fluid MIC-1 is derived from the fetal membranes and decidua, but that MIC-1 is unlikely to be involved in the pathophysiology of preterm birth or premature rupture of membranes
- Treating DU145 prostate cancer cells with MIC-1 causes loss of adhesion and consequently induces cell detachment and apoptosis. This is mediated at least in part by reduction in metallothionein 1E, RhoE and catenin delta 1.
- NAG-1 may be involved in differentiation and apoptotic processes of nasal epithelial cells. It is still unclear whether NAG-1 is an inducer or a byproduct of differentiation or apoptosis
- expression of NAG-1 by troglitazone requires the early growth response gene EGR-1
- Serum MIC-1 levels are markedly depressed in women, some weeks before miscarriage and at a time when the fetus is still viable. This suggests possible predictive and causative roles, as well as therapeutic potential
- MIC-1 has a role in progression of primary pancreatic cancers, intraductal papillary mucinous neoplasms, and pancreatic cancer
- The combination of serum levels of MIC-1 and CA19-9 significantly improved diagnostic accuracy of pancreatic cancer (sensitivity, 70%; specificity, 85%)
- This study shows an association between a nonsynonymous change (H6D) in the MIC-1 gene and prostate cancer. This finding supports the hypothesis that genetic variation in the inflammatory process contributes to prostate cancer susceptibility
- Findings suggest that early prostate carcinogenesis is associated with expression of mature GDF15 protein.
- The results suggest that I3C represses cell proliferation through up-regulation of NAG-1 and that ATF3 may play a pivotal role in DIM-induced NAG-1 expression in human colorectal cancer cells.
- expression levels may serve as a surrogate marker for the AKT activation in tumors
- NAG-1 expression is up-regulated by TPA in LNCaP cells through a PKC-dependent pathway involving the activation of NF-kappa B
- GDF-15 induction is an immediate early response to liver injury that can occur through TNF and p53 independent pathways
- t10,c12-CLA stimulates ATF3/NAG-1 expression and subsequently induces apoptosis in an isomer specific manner
- An additional serum marker for the detection of prostatic cancer.
- GDF-15 expression increased within 12 hours of symptom onset and remained upregulated for at least 2 weeks after myocardial infarct.
- highly expressed in the placenta and the prostate, but not normally in many other organs, including the heart
- Study suggests that proapoptotic activity of NAG-1 is cell type specific and not related to COX-2 expression.
- Induction of message and protein in prostate cancer cells requires 1alpha, 25-dihydroxyvitamin D3.
- Single Nucleotide Polymorphisms in Macrophage inhibitory cytokine-1 is associated with prostate cancer
- Stimulation of macrophage inhibitory cytokine 1-dependent S phase arrest in normal gut epithelial cells might help to revitalize the clinical use of N-phosphonacetyl-l-aspartate, which has been limited by gut toxicity
- Serum levels of MIC-1 and MIC-1 genotype may be clinically useful in the management of rheumatoid arthritis as well as in selection of patients for hemopoietic stem cell transplantation, since they predict disease course and response to therapy.
- study does not support the role of common genetic variation at MIC1 and IL1RN in prostate cancer susceptibility
- TAp63-dependent induction of growth differentiation factor 15 (GDF15) plays a critical role in the regulation of keratinocyte differentiation.
- GDF15 overexpression arising from an expanded erythroid compartment contributes to iron overload in thalassemia syndromes by inhibiting hepcidin expression.
- growth differentiation factor 15 has a role in molecular alterations in prostate carcinomas resulting from exposure to chemotherapy
- The induction of GDF15 and STC2 is likely specific to MK-4, vitamin K2 analog.
- Transgenic mice overexpressing MIC-1 show hypophagia and weight loss; sera from subjects with advanced prostate cancer show a direct correlation between MIC-1 abundance and cancer-associated weight loss, defining MIC-1 as a central regulator of appetite.
- The NAG-1 was expressed strongly in intestinal metaplasia and adenoma, and inversely correlated to tumor stages
- There is a possible role for macrophage-inhibiting cytokine-1 (MIC-1) in coronary artery cardiovascular events.
- Microarray studies show that our in vitro model system reflects many cellular and molecular alterations characteristic of cervical cancer, and identified SIX1 and GDF15 as 2 novel potential biomarkers of cervical cancer progression.
- GDF-15 does not decrease proliferation of glioblastoma cell lines, while its effects on invasiveness are not consistent.
- GDF15 is normal in most superdonors, indicating that GDF15 overexpression arising from the expanded erythroid pool necessary to replace donated red cells is not the biochemical mechanism for the decreased serum hepcidin
- MIC-1 may function to promote development of more aggressive melanoma tumors
- trichostatin A-induced NAG-1 expression involves multiple mechanisms at the transcriptional and post-transcriptional levels.
- CDA I patients express very high levels of serum GDF15, and GDF15 contributes to the inappropriate suppression of hepcidin with subsequent secondary hemochromatosis.
- GDF15 can be induced by pathophysiologic changes in iron availability, raising important questions about the mechanism of regulation and its role in iron homeostasis
- MIC-1 was obviously overexpressed in gastric cancers and MIC-1 secretion into blood may be useful for the prediction of gastric cancer progression.