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Validated All-in-One™ qPCR Primer for JUND(NM_005354.5) Search again
Product ID:
HQP117779
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AP-1
Gene Description:
JunD proto-oncogene, AP-1 transcription factor subunit
Target Gene Accession:
NM_005354.5(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
The protein encoded by this intronless gene is a member of the JUN family, and a functional component of the AP1 transcription factor complex. It has been proposed to protect cells from p53-dependent senescence and apoptosis. Alternate translation initiation site usage results in the production of different isoforms. [provided by RefSeq].
Gene References into function
- An alternative model of H ferritin promoter transactivation by c-Jun
- JunD activated by LHRH acts as a modulator of cell proliferation and cooperates with the anti-apoptotic and anti-mitogenic functions of LHRH.
- junD activation by ultraviolet rays plays a role in apoptosis in myeloblastic leukemia ML-1 cells
- Translation initiation from alternative AUG and non-AUG sites in human, mouse and rat.
- Constitutive activation of nuclear factor kappaB p50/p65 and Fra-1 and JunD is essential for deregulated interleukin 6 expression in prostate cancer.
- Menin is important for recruiting an mSin3A-histone deacetylase complex to repress JunD transcriptional activity.
- Data show that human T-cell leukemia virus type I (HTLV-I) bZIP factor can activate JunD-dependent transcription and that its amino-terminus is required.
- c-jun, junD, junB, and c-fos and Notch2 are expressed in splenic marginal zone lymphoma
- menin suppresses osteoblast maturation, in part, by inhibiting the differentiation actions of JunD
- JunD is another ARE regulatory protein for transcriptional activation of the human ferritin H gene and probably other antioxidant genes containing the conserved ARE sequences by which JunD may confer cytoprotection during oxidative stress
- JunD limits cardiomyocyte hypertrophy and protects the pressure-overloaded heart from cardiac apoptosis
- Menin's dynamic regulation of histone modifiers with JunD is responsible for PKC theta-synergistic effect on Nur77 expression in T cell
- JunB and JunD contribute opposing effects; JunB activated whereas JunD repressed heme oxygenase-1 expression in human renal epithelial cells
- Pyk2 regulation is associated with increased expression of Fra-1 and JunD, activator protein-1 transcription factors known to be required for involucrin expression.
- Coordinated down- and up-regulation of the various AP-1 subunits in the course of epidermal wound healing is important for its undisturbed progress, putatively by influencing inflammation and cell-cell communication.
- Our data suggest that JUND and CLDN4 are critical mediators of the antiproliferative and antiviral effects of type I IFNs and further confirm the functional importance of the DNA-binding domain of Stat2.
- Dimerization with the Jun proteins inhibits c-Fos nuclear exit.
- aberrantly expressed Fra-2 in association with JunD may play a major role in CCR4 expression and oncogenesis in adult t-cell leukemia.
- evidence is provided that HBZ/JunD heterodimers interact with Sp1 transcription factors and that activation of hTERT transcription by these heterodimers is mediated through binding sites for Sp1 present in the hTERT promoter.
- Damaging exercise induced the expression of capZalpha, MCIP1, CARP1, DNAJB2, c-myc, and junD, each of which are likely involved in skeletal muscle growth, remodeling, and stress management.
- JunD overexpression increases production of reactive oxygen species in LNCaP cells in a low androgen environment.
- JunD is a major determinant of macrophage activity and is associated with glomerulonephritis susceptibility.
- JunD activation reduces the proliferation of cancer cells.
- JunD is a biological suppressor of ZO-1 expression in intestinal epithelial cells and plays a critical role in maintaining epithelial barrier function
- These results reveal the molecular bases of the expression specificity of PADI1 and PADI3 during keratinocyte differentiation through a long-range enhancer and support a model of PADI gene regulation depending on c-Jun-JunD competition.