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AP-1(c-Jun/FosB (show FOSB ELISA Kits)) 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 (show TLX3 ELISA Kits) and modulated transcription and regulated neurotransmitter phenotype via its transactivation domain
Data show that JNK (show MAPK8 ELISA Kits) signalling inhibits the growth of losers, while JAK (show JAK3 ELISA Kits)/STAT (show STAT1 ELISA Kits) signalling promotes competition-induced winner cell proliferation.
Mir (show MYLIP ELISA Kits)-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 (show EGFR ELISA Kits)) pathway in the lateral epidermis for sustained dpp (show TGFb ELISA Kits) expression in the LE. Specifically, we demonstrate that Egfr (show EGFR ELISA Kits) pathway activity in the lateral epidermis prevents expression of the gene scarface (scaf), encoding a secreted antagonist of JNK (show MAPK8 ELISA Kits) signaling
Tau and spectraplakin promote synapse formation and maintenance through Jun kinase (show MAPK9 ELISA Kits) and neuronal trafficking.
n addition to significantly increasing the number of JNK (show MAPK8 ELISA Kits) target genes identified so far, our results reveal that the LE is a highly heterogeneous morphogenetic organizer, sculpted through crosstalk between JNK (show MAPK8 ELISA Kits), 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 (show SCRIB ELISA Kits)) tumors requires bZIP protein Fos, the ETS (show ETS1 ELISA Kits)-domain factor Ets21c and the nuclear receptor Ftz-F1 (show NR5A2 ELISA Kits), all acting downstream of Jun-N-terminal kinase (show MAPK8 ELISA Kits).
Diminished MTORC1-dependent JNK (show MAPK8 ELISA Kits) activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
ROS (show ROS1 ELISA Kits)/JNK (show MAPK8 ELISA Kits)/p38 (show MAPK14 ELISA Kits)/Upd (show UROD ELISA Kits) 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 (show MAPK8 ELISA Kits) pathway is responsible for the majority of the phenotypes and transcriptional changes downstream of Notch (show NOTCH1 ELISA Kits)-Src (show SRC ELISA Kits) synergy.
This study demonstrated that the mechanism by which Bsk (show FRK ELISA Kits) is required for pruning is through reducing the membrane levels of the adhesion molecule (show NCAM1 ELISA Kits) Fasciclin II (show NCAM2 ELISA Kits) (FasII)
Porcine reproductive and respiratory syndrome virus -activated TAK-1 (show NR2C2 ELISA Kits) was essential for the activation of JNK (show MAPK8 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) pathways and IL-8 (show IL8 ELISA Kits) 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 (show ICAM1 ELISA Kits) and IL10 (show IL10 ELISA Kits) 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 (show CA2 ELISA Kits)+) signaling pathway increases Nr4a1 (show NR4A1 ELISA Kits) expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2 (show MEF2C ELISA Kits), AP1, and CREB (show CREB1 ELISA Kits) transcription factors thus demonstrating an important interplay between the Ca(2 (show CA2 ELISA Kits)+) and cAMP pathways in regulating Nr4a1 (show NR4A1 ELISA Kits) expression.
we performed cotransfections of AP-1 expression plasmids with different mouse Gja1 (show GJA1 ELISA Kits) promoter/luciferase reporter constructs within TM3 (show TPM1 ELISA Kits) Leydig and TM4 (show TPM4 ELISA Kits) Sertoli cells.We showed that a functional cooperation between cJun and cFos activates Gja1 (show GJA1 ELISA Kits) 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 (show MEF2C ELISA Kits) and AP-1 confer antagonistic regulation of Hspb7 (show HSPB7 ELISA Kits) gene expression in skeletal muscle, with implications for autophagy and muscle atrophy.
results suggest that fibroblasts, c-Jun, and IGF-1 (show IGF1 ELISA Kits) 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 (show TLR4 ELISA Kits)-NOS1 (show NOS1 ELISA Kits)-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 (show ATP6V0D1 ELISA Kits) is the underlying mechanism that accommodates the increased functional requirement of Cdk5 (show CDK5 ELISA Kits) activation during neuronal differentiation. In addition, we demonstrated that p39 (show ATP6V0D1 ELISA Kits) selectively directs Cdk5 (show CDK5 ELISA Kits) to phosphorylate protein substrates essential for axonal development, dendritic spine formation, and synaptogenesis. Moreover, our studies suggest opposing roles o
NF-kappaB (show NFKB1 ELISA Kits) and c-Jun coregulate lipopolysaccharide-induced Fra-1 (show FOSL1 ELISA Kits) transcription.
AP-1 (show FOSB ELISA Kits) 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 (show NR1H4 ELISA Kits)/FAK (show PTK2 ELISA Kits)/c-Jun axis to upregulate MUC4 (show MUC4 ELISA Kits) 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 (show GABPA ELISA Kits), ATF4 (show ATF4 ELISA Kits), 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 (show NFKB1 ELISA Kits) (RelB (show RELB ELISA Kits)/p52 (show FKBP4 ELISA Kits)) downstream of MEK (show MAP2K1 ELISA Kits)-ERK (show EPHB2 ELISA Kits) and NIK (show MAP3K14 ELISA Kits)-IKK-alpha (show CHUK ELISA Kits)-NF-kappaB2 (p100 (show CUX1 ELISA Kits)) phosphorylation, respectively was responsible for persistent Ccl20 (show CCL20 ELISA Kits) 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 (show MAPK8 ELISA Kits), AP-1 (show FOSB ELISA Kits), and CHOP (show DDIT3 ELISA Kits) 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 (show TRIM69 ELISA Kits) in the development of the zebrafish brain through ap-1 pathway.
CPEB-1 (show CPEB1 ELISA Kits) 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 (show Vcan ELISA Kits) synthesis in the presence of IL-1beta (show IL1B ELISA Kits) 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