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Validated All-in-One™ qPCR Primer for JUNB(NM_002229.2) Search again
Product ID:
HQP009854
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AP-1
Gene Description:
JunB proto-oncogene, AP-1 transcription factor subunit
Target Gene Accession:
NM_002229.2(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:
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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
- JunB is an important regulator of erythroid differentiation
- JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction
- Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B.
- demonstrated that a functional AP-1 site mediates MMP-2 transcription in cardiac cells through the binding of distinctive Fra1-JunB and FosB-JunB heterodimers. The synthesis of MMP-2 is considered to be independent of the AP-1 transcriptional complex
- results have revealed, for the first time, amplification and expression patterns of JUNB in primary cutaneous lymphomas
- Real-time RT-PCR gave further insights into the role of JunB in human CML. The expression levels were significantly impaired in CML cases. In the promoter area, most of the CpG sites were methylated only in CML cases.
- C/EBPalpha and PKC/delta affect expression of this gene and monocyte differentiation.
- Expression of junB was induced by TPA and Saikosaponin a during 30 min to 6 h of treatment.
- JunB was strongly expressed in T-cell lymphomas, but non-Hodgkin B-cell lymphomas do not or only weakly express JunB.
- Transcription factor c-Jun plays a principal role in down-regulation of mdr-1 expression and induction of apoptosis in salvicine-treated human MDR K562/A02 cells.
- c-jun, junD, junB, and c-fos and Notch2 are expressed in splenic marginal zone lymphoma
- The IGFBP3, hRas, JunB, Egr-1, Id1 and MIDA1 genes were up-regulated in psoriatic involved skin compared with uninvolved skin.
- 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole sensitivity-inducing factor (DSIF)- and NELF-mediated transcriptional pausing has a dual function in regulating immediate-early expression of the human junB gene.
- JunB and JunD contribute opposing effects; JunB activated whereas JunD repressed heme oxygenase-1 expression in human renal epithelial cells
- results suggest that HTLV-I HBZ-SP1- mediated sequestration of JunB to the HBZ-SP1 nuclear bodies may be causing the repression of JunB activity in vivo
- 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.
- Dimerization with the Jun proteins inhibits c-Fos nuclear exit.
- JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas.
- constitutive action of aberrantly expressed JunB on hypomethylated CD30 CpG islands of lymphocytes triggers CD30 induction and initiates activation of the JunB-CD30-JunB loop, essential to the pathogenesis of HL and ALCL
- JunB levels, which are high in S phase, drop during mid- to late G2 phase due to accelerated phosphorylation-dependent degradation by the proteasome, and are required for subsequent reduction of cyclin A2 levels in prometaphase
- sumoylation of JunB regulates its ability to induce cytokine gene transcription and likely plays a critical role in T cell activation.
- JunB plays an important role in controlling prostate carcinogenesis and may be a new target for cancer prevention and therapy.
- results establish a role for JunB in normal erythropoiesis and indicate that JunB may play a major role in the development of JAK2 V617F myeloproliferative disorders.