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