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AP-1(c-Jun/FosB (Montrer FOSB Kits ELISA)) may play a role in neurogenesis via the induction of FoxD5b expression during early vertebrate development
The cJun transcription factor bound to a variant cAMP response element in the promoter region of tlx3 (Montrer TLX3 Kits ELISA) and modulated transcription and regulated neurotransmitter phenotype via its transactivation domain
Data show that JNK (Montrer MAPK8 Kits ELISA) signalling inhibits the growth of losers, while JAK (Montrer JAK3 Kits ELISA)/STAT (Montrer STAT1 Kits ELISA) signalling promotes competition-induced winner cell proliferation.
Mir (Montrer MYLIP Kits ELISA)-8 modulates Drosophila C virus replication by negative regulation of dJun.
Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr (Montrer EGFR Kits ELISA)) pathway in the lateral epidermis for sustained dpp (Montrer TGFb Kits ELISA) expression in the LE. Specifically, we demonstrate that Egfr (Montrer EGFR Kits ELISA) pathway activity in the lateral epidermis prevents expression of the gene scarface (scaf), encoding a secreted antagonist of JNK (Montrer MAPK8 Kits ELISA) signaling
Tau and spectraplakin promote synapse formation and maintenance through Jun kinase (Montrer MAPK9 Kits ELISA) and neuronal trafficking.
n addition to significantly increasing the number of JNK (Montrer MAPK8 Kits ELISA) target genes identified so far, our results reveal that the LE is a highly heterogeneous morphogenetic organizer, sculpted through crosstalk between JNK (Montrer MAPK8 Kits ELISA), segmental and AP signalling. This fine-tuning regulatory mechanism is essential to coordinate morphogenesis and dynamics of tissue sealing
malignant transformation of the ras(V12)scrib(1 (Montrer SCRIB Kits ELISA)) tumors requires bZIP protein Fos, the ETS (Montrer ETS1 Kits ELISA)-domain factor Ets21c and the nuclear receptor Ftz-F1 (Montrer NR5A2 Kits ELISA), all acting downstream of Jun-N-terminal kinase (Montrer MAPK8 Kits ELISA).
Diminished MTORC1-dependent JNK (Montrer MAPK8 Kits ELISA) activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
ROS (Montrer ROS1 Kits ELISA)/JNK (Montrer MAPK8 Kits ELISA)/p38 (Montrer MAPK14 Kits ELISA)/Upd (Montrer UROD Kits ELISA) stress responsive module restores tissue homeostasis. This module is not only activated after cell death induction but also after physical damage and reveals one of the earliest responses for imaginal disc regeneration.
Significantly, the JNK (Montrer MAPK8 Kits ELISA) pathway is responsible for the majority of the phenotypes and transcriptional changes downstream of Notch (Montrer NOTCH1 Kits ELISA)-Src (Montrer SRC Kits ELISA) synergy.
This study demonstrated that the mechanism by which Bsk (Montrer FRK Kits ELISA) is required for pruning is through reducing the membrane levels of the adhesion molecule (Montrer NCAM1 Kits ELISA) Fasciclin II (Montrer NCAM2 Kits ELISA) (FasII)
Porcine reproductive and respiratory syndrome virus -activated TAK-1 (Montrer NR2C2 Kits ELISA) was essential for the activation of JNK (Montrer MAPK8 Kits ELISA) and NF-kappaB (Montrer NFKB1 Kits ELISA) pathways and IL-8 (Montrer IL8 Kits ELISA) expression.
The effects of prostaglandin F2alpha administration on transcription factor AP-1 expression and the expression of downstream genes involved in luteolysis are reported.
ICAM1 (Montrer ICAM1 Kits ELISA) and IL10 (Montrer IL10 Kits ELISA) were upregulated in ventilator-induced lung injury. Nuclear transcription factor AP-1 may be responsible for this upregulation.
Taken together, these findings indicate that LT reduces c-Jun protein levels via two distinct mechanisms, thereby inhibiting critical cell functions, including cellular proliferation.
Ca(2 (Montrer CA2 Kits ELISA)+) signaling pathway increases Nr4a1 (Montrer NR4A1 Kits ELISA) expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2 (Montrer MEF2C Kits ELISA), AP1, and CREB (Montrer CREB1 Kits ELISA) transcription factors thus demonstrating an important interplay between the Ca(2 (Montrer CA2 Kits ELISA)+) and cAMP pathways in regulating Nr4a1 (Montrer NR4A1 Kits ELISA) expression.
we performed cotransfections of AP-1 expression plasmids with different mouse Gja1 (Montrer GJA1 Kits ELISA) promoter/luciferase reporter constructs within TM3 (Montrer TPM1 Kits ELISA) Leydig and TM4 (Montrer TPM4 Kits ELISA) Sertoli cells.We showed that a functional cooperation between cJun and cFos activates Gja1 (Montrer GJA1 Kits ELISA) expression and requires an AP-1 DNA regulatory element located between -132 and -26 bp
AP1 factors are important regulators of adult taste cell renewal and their downregulation negatively impacts taste maintenance.
these data indicate that MEF2 (Montrer MEF2C Kits ELISA) and AP-1 confer antagonistic regulation of Hspb7 (Montrer HSPB7 Kits ELISA) gene expression in skeletal muscle, with implications for autophagy and muscle atrophy.
results suggest that fibroblasts, c-Jun, and IGF-1 (Montrer IGF1 Kits ELISA) play key roles in mediating stromal-epithelial interactions that are required for the therapeutic effects of finasteride in benign prostate epithelial cells
These findings highlight a key role of the TLR4 (Montrer TLR4 Kits ELISA)-NOS1 (Montrer NOS1 Kits ELISA)-AP1 signaling axis in regulating macrophage polarization
Data suggest that Sf1 and c-jun interact and cooperate to activate the Fdx1 promoter in MA-10 (tumorigenic cell line) and TM3 (non-tumorigenic cell line) Leydig cells; such activation requires different regulatory elements located between -124 and -306 bp of Fdx1 promoter and involves recruitment of Sf1 to this region. (Sf1 = splicing factor 1; c-jun = proto-oncogene c-jun; Fdx1 = ferredoxin 1)
In this study, we discovered that selective upregulation of p39 (Montrer ATP6V0D1 Kits ELISA) is the underlying mechanism that accommodates the increased functional requirement of Cdk5 (Montrer CDK5 Kits ELISA) activation during neuronal differentiation. In addition, we demonstrated that p39 (Montrer ATP6V0D1 Kits ELISA) selectively directs Cdk5 (Montrer CDK5 Kits ELISA) to phosphorylate protein substrates essential for axonal development, dendritic spine formation, and synaptogenesis. Moreover, our studies suggest opposing roles o
NF-kappaB (Montrer NFKB1 Kits ELISA) and c-Jun coregulate lipopolysaccharide-induced Fra-1 (Montrer FOSL1 Kits ELISA) transcription.
AP-1 (Montrer FOSB Kits ELISA) likely plays a more important role in the AR cistrome in fibroblasts.
elevated levels of bile acid increase the tumorigenic potential of pancreatic cancer cells by inducing FXR (Montrer NR1H4 Kits ELISA)/FAK (Montrer PTK2 Kits ELISA)/c-Jun axis to upregulate MUC4 (Montrer MUC4 Kits ELISA) expression.
Immunohistochemistry was employed to analyze cFos, cJun and CD147 expression in 41 UCB cases and 34 noncancerous human bladder tissues.
Expression of either dominant-negative or constitutively active mutants of Nrf2 (Montrer GABPA Kits ELISA), ATF4 (Montrer ATF4 Kits ELISA), or c-Jun confirmed that distinct transcription units are regulated by these transcription factors.
mutually exclusive transcriptional regulation by AP-1 (cjun/cfos) and non-canonical NF-kappaB (Montrer NFKB1 Kits ELISA) (RelB (Montrer RELB Kits ELISA)/p52 (Montrer FKBP4 Kits ELISA)) downstream of MEK (Montrer MAP2K1 Kits ELISA)-ERK (Montrer EPHB2 Kits ELISA) and NIK (Montrer MAP3K14 Kits ELISA)-IKK-alpha (Montrer CHUK Kits ELISA)-NF-kappaB2 (p100 (Montrer CUX1 Kits ELISA)) phosphorylation, respectively was responsible for persistent Ccl20 (Montrer CCL20 Kits ELISA) expression in the colonic cells.
Glucocorticoid receptor (GR) is recruited to activator protein-1 (AP-1) target genes in a DNA-binding-dependent manner.
These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK (Montrer MAPK8 Kits ELISA), AP-1 (Montrer FOSB Kits ELISA), and CHOP (Montrer DDIT3 Kits ELISA) may interfere with complete autophagy.
Overall, our results suggest that miR-4632 plays an important role in regulating HPASMC proliferation and apoptosis by suppression of cJUN, providing a novel therapeutic miRNA candidate for the treatment of pulmonary vascular remodeling diseases. It also implies that serum miR-4632 has the potential to serve as a circulating biomarker for PAH diagnosis.
Findings suggest that AP-1 factors are regulators of RNA polymerase III (Pol III)-driven 5S rRNA and U6 snRNA expression with a potential role in cell proliferation.
These results support a role for trim69 (Montrer TRIM69 Kits ELISA) in the development of the zebrafish brain through ap-1 pathway.
CPEB-1 (Montrer CPEB1 Kits ELISA) control of c-Jun mRNA translation regulates GH gene expression and resulting downstream signaling events (e.g., synaptic plasticity) in the mouse hippocampus.
The present data indicate that bovine dialyzable leukocyte extract can block the AP-1 DNA-binding activity and expression of several transcriptions factors in breast cancer cells.
dynamic compression stimulates cell proliferation and proteoglycan (Montrer Vcan Kits ELISA) synthesis in the presence of IL-1beta (Montrer IL1B Kits ELISA) and/or inhibitors of the MAPKs and NFkappaB and AP-1 signalling pathways
This gene is the putative transforming gene of avian sarcoma virus 17. It encodes a protein which is highly similar to the viral protein, and which interacts directly with specific target DNA sequences to regulate gene expression. This gene is intronless and is mapped to 1p32-p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Jun activation domain binding protein
, activator protein 1
, enhancer-binding protein AP1
, jun oncogene
, proto-oncogene c-Jun
, transcription factor AP-1
, v-jun avian sarcoma virus 17 oncogene homolog
, v-jun sarcoma virus 17 oncogene homolog
, Avian sarcoma virus 17 (v-jun) oncogene homolog
, Jun oncogene
, V-jun avian sarcoma virus 17 oncogene homolog
, proto-oncogene c-jun
, CDK5 activator 2
, cyclin-dependent kinase 5 activator 2
, cyclin-dependent kinase 5 regulatory subunit 2
, v-jun sarcoma virus 17 oncogene
, JUN kinase
, Jun N-terminal kinase
, Jun NH2-terminal kinase
, Jun-N-terminal kinase
, c-Jun N-terminal kinase
, c-Jun aminoterminal kinase
, c-Jun-N-terminal kinase
, drosophila JNK
, immediate early
, jun A
, Jun related antigen
, complementation group V
, LOW QUALITY PROTEIN: transcription factor AP-1