|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for MAP2K4(NM_003010.3) Search again
Product ID:
HQP016830
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
JNKK, JNKK1, MAPKK4, MEK4, MKK4, PRKMK4, SAPKK-1, SAPKK1, SEK1, SERK1, SKK1
Gene Description:
mitogen-activated protein kinase kinase 4
Target Gene Accession:
NM_003010.3(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:
|
|
| A | B |
|
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. |
|
Summary
This gene encodes a dual specificity protein kinase that belongs to the Ser/Thr protein kinase family. This kinase is a direct activator of MAP kinases in response to various environmental stresses or mitogenic stimuli. It has been shown to activate MAPK8/JNK1, MAPK9/JNK2, and MAPK14/p38, but not MAPK1/ERK2 or MAPK3/ERK3. This kinase is phosphorylated, and thus activated by MAP3K1/MEKK. The knockout studies in mice suggested the roles of this kinase in mediating survival signal in T cell development, as well as in the organogenesis of liver. [provided by RefSeq].
Gene References into function
- There appears to be consistent rate of genetic inactivation of MAP2K4 among most tumor types, including breast cancer.
- JNK-dependent phosphorylation and thus inactivation of Mcl-1 may be one of the mechanisms through which oxidative stress induces cellular damage
- Jun N-terminal kinase has a role in IL-4 induction
- Ubiquitylation of MEKK1 inhibits its phosphorylation of MKK1 and MKK4 and activation of the ERK1/2 and JNK pathways
- in the setting of wild-type PTEN, PI3K- and MKK4/JNK-dependent pathways cooperate to maintain cell survival.
- regulation of fibroblast functions important for wound healing by basal JNK activity
- docking site in MKK4 mediates high affinity binding to JNK MAPKs and competes with similar docking sites in JNK substrates
- JNK, MKK-4, and MKK-7 form an active signaling complex in rheumatoid arthritis and this novel JNK signalsome is activated in response to IL-1 and migrates to the nucleus
- JNK and p38 MAPK activities in UVA-induced signaling pathways leading to AP-1 activation and c-Fos expression
- MMP-9 inhibition activity of resveratrol and its inhibition of JNK and PKC-delta may have a therapeutic potential in cancer.
- Apoptosis signaling triggered by ascididemin is routed via CASP2 and JNKK to mitochondria.
- save th
- AP-1 and JNK have roles in reactive oxygen species activation in tobacco-induced mucin production in lung cells
- PP5 plays an important role in the survival of cells in a low oxygen environment by suppressing a hypoxia-induced ASK-1/MKK4/JNK signaling cascade that promotes an apoptotic response
- CYLD has a role in megative regulation of JNK signaling
- Our investigations revealed significantly reduced mRNA expression of metastases suppressor gene Mkk4 in breast cancer brain metastasis.
- Loss of Mkk4 protein expression is associated with pancreatic carcinoma progression
- Taken together, our data suggested that the JNK/c-Jun signaling cascade plays a crucial role in Cd-induced neuronal cell apoptosis and provides a molecular linkage between oxidative stress and neuronal apoptosis.
- Pharmacological inhibition of oxidative stress diminished the elevated p38, JNK activity and PARP cleavage, and enhanced PD cybrid viability.
- JIP1 and JIP3, have a cross-talk that leads to the regulation of the ASK1-SEK1-JNK signal during glucose deprivation; cross-talk between JIP3 and JIP1 is mediated through SEK1-JNK2 and Akt1.
- Our results demonstrate that radioresistance of Saos2 osteosarcoma cells is due to NFkappaB-mediated inhibition of JNK
- an independent role for p38 MAPK and JNK in LPA-induced IL-8 expression and secretion via NF-kappaB and AP-1 transcription respectively in human bronchial epithelial cells.
- These results indicate that SPC stimulates the proliferation of hADSCs through the Gi/Go-PLC-JNK pathway and that LPA receptors may be responsible in part for the SPC-induced proliferation
- The present study demonstrates that HSP cells compared to controls are more sensitive to DNA damages induced by H2O2 treatment, and that JNK phosphorylation levels are increased in HSP fibroblasts after hydrogen peroxide and serum stimuli.
- Homozygous deletion or reduced expression of MKK4 may contribute to the development of ovarian serous carcinoma.
- Bax is phosphorylated by stress-activated JNK and/or p38 kinase and phosphorylation of Bax leads to mitochondrial translocation prior to apoptosis
- JNK (c-Jun N-terminal kinase) function might be modulated by targeting MKK-7 to suppress cytokine-mediated fibroblast-like synoviocytes (FLS) activation while leaving other stress responses intact.
- p38 MAPK and JNK pathways play an important role in VEGF secretion from malignant glioma cells under normoxic conditions.
- Phosphorylated forms of MKK4, JNK, and c-Jun were detected in salivary infiltrating mononuclear cells in Sjogren's syndrome patients
- MKK4 decreases phosphatase and tensin homologue deleted from chromosome 10 (PTEN) and promotes survival in non-small-cell lung cancer (NSCLC) cells.
- LMP1-mediated DNA methyltransferase-1 (DNMT1) activation involves JN kinase.
- The results suggest that JNK regulates human iNOS expression by stabilizing iNOS mRNA possibly by a tristetraprolin -dependent mechanism.
- TNF-induced TRAF2-RIP1-AIP1-ASK1 complex formation and for the activation of ASK1-JNK/p38 apoptotic signaling.
- PF4-stimulated immediate monocyte functions (oxygen radical formation) are regulated by p38 MAPK, Syk, and PI3K, whereas delayed functions (survival and cytokine expression) are controlled by Erk and JNK.
- Cytosolic mRNA is shifted toward active polysomes in prostate tumor cells with higher levels of MKK4 protein, suggesting that MKK4 mRNA is translated more efficiently in these cells.
- JNK3 recruits MKK4 to the beta-arrestin-2 scaffold complex by binding to the MAPK docking domain (D-domain) located within the N terminus of MKK4.
- Disruption of signaling through MKK4 yields differential response in hypoxic colon cancer cells treated with oxaliplatin.
- JNK is differentially regulated by MKK4 and MKK7 depending on the stimulus.
- the molecular interactions of arrestin2 and arrestin3 and their individual domains with the components of the two MAPK cascades, ASK1-MKK4-JNK3 and c-Raf-1-MEK1-ERK2
- multiple copy number alterations in chromosome regions implicated in malignancy progression and indicated a strong expression of MAP2K4 and MCL1 genes in rhabdomyosarcoma