Repression of AP-1 Function: A Mechanism for the Regulation of Blimp-1 Expression and B Lymphocyte Differentiation by the B Cell Lymphoma-6 Protooncogene1.
Function and regulation of AP-1 subunits in skin physiology and pathology. The mouse skin has become the model of choice to study the regulation and function.
AP-1 function and regulation Michael Karin*. Regulation and function of AP-1 genes The regulation of AP-1 activity occurs at two major levels.
- AP-1 function and regulation Karin, Michael; Liu, Zheng-gang. 20% off on PDF purchases; Organize your research; Get updates on your journals and topic searches.
- AP-1 function and regulation. Karin M(1). of AP-1 factors in functions such as cell proliferation. signaling pathways involved in the regulation of AP-1.
- Function and regulation of AP-1 subunits in skin physiology and pathology. The mouse skin has become the model of choice to study the regulation and function of.
- 240 AP-1 function and regulation Michael. Liu and Zandi 241 Regulation and function of AP-1 genes The regulation of AP-1 activity. Purchase PDF |.
- Page 1. 240 AP-1 function and regulation Michael Karin*, Zheng-gang Liu and Ebrahim Zandi AP-1 (activating protein-1) is a collective term referring.
AP- 1 function and regulation Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by Ro. MEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable. Source Available from: journals. AP- 1 is a common intracellular transcription activator [2.
Previous studies have shown that AP- 1 participates in many important cellular activities, including cell differentiation, cell proliferation and apoptosis [3. In addition, the up- regulation of AP- 1 has also been found to be related to tumorigenesis [3. Show abstract][Hide abstract]ABSTRACT: With the rapid development in nanotechnology, nickel nanoparticles (Ni NPs) have emerged in the application of nanomedicine in recent years. However, the potential adverse health effects of Ni NPs are unclear.
In this study, we examined the inhibition effects of epigallocatechin- 3- gallate (EGCG) on the toxicity induced by Ni NPs in mouse epidermal cell line (JB6 cell). MTT assay showed that Ni NPs induced cytotoxicity in a dose- dependent manner while EGCG exerted a certain inhibition on the toxicity. Additionally, EGCG could reduce the apoptotic cell number and the level of reactive oxygen species (ROS) in JB6 cells induced by Ni NPs. Furthermore, we observed that EGCG could down- regulate Ni NPs- induced activator protein- 1 (AP- 1) and nuclear factor- κB (NF- κB) activation in JB6 cells, which has been shown to play pivotal roles in tumor initiation, promotion and progression. Western blot indicated that EGCG could alleviate the toxicity of Ni NPs through regulating protein changes in MAPK signaling pathways. In summary, our results suggest that careful evaluation on the potential health effects of Ni NPs is necessary before being widely used in the field of nanomedicine.
Inhibition of EGCG on Ni NPs- induced cytotoxicity in JB6 cells may be through the MAPK signaling pathways suggesting that EGCG might be useful in preventing the toxicity of Ni NPs. Full- text · Article · Mar 2.
PLo. S ONE Source Available from: Elias Oziolor "The high expression of Jun. B in colon derived, NCM4. Caco- 2 and T8. 4 cells (not shown) correlated with low IL- 6 secretion from these transformed cell lines supporting its' role as a transcription repressor of the IL- 6 gene. In fact Jun. B is often considered a transcriptional repressor or a poor activator despite its direct role in the induction of cytokines like IL- 2, IL- 4, VEGF and cyclin A in various cellular contexts[1.
The mechanism is likely associated with its' antagonism of c. Jun. " [Show abstract][Hide abstract]ABSTRACT: The innate immune response is characterized by activation of transcription factors, nuclear factor kappa B and activator protein- 1 and their downstream targets, the pro- inflammatory cytokines including interleukin 1β and interleukin 6. Normal development of this response in the intestine is critical to survival of the human neonate and delays can cause the onset of devastating inflammatory diseases such as necrotizing enterocolitis. Previous studies have addressed the role of nuclear factor kappa B in the development of the innate immune response in the enterocyte, however despite its central role in the control of multiple pro- inflammatory cytokine genes, little is known on the role of Activator Protein 1 in this response in the enterocyte. Here we show that the canonical Activator Protein 1 members, c. Jun and c. Fos and their upstream kinases JNK and p.
Our data supports a model whereby the c. Fos/c. Jun heterodimer and the more potent c. Jun homodimer downstream of JNK are replaced by less efficient Jun.
D containing dimers, contributing to the decreased responsiveness to interleukin 1β and decreased interleukin 6 secretion observed in the mature enterocyte. The tissue specific expression of Jun. B in colonocytes and colon derived tissues together with its ability to repress Interleukin- 1β induction of an Interleukin- 6 gene reporter in the NCM- 4. Jun. B containing dimers may offer an attractive therapeutic strategy for the control of IL- 6 secretion during inflammatory episodes in this area of the intestine.
Full- text · Article · Jan 2. PLo. S ONE Source Available from: Ewelina Szymanska "levels of c- Jun and induces its Ser. AP- 1 transcriptional activity can result from increased abundance of AP- 1 subunits in the nucleus or from their post- translational modifications which enhance their dimerization and DNA- binding abilities[3. To examine which of these mechanisms could underlie the increase of the AP- 1 reporter activity upon Dyn. AP- 1 subunits: c- Jun, Jun.
B, Jun. D and c- Fos (they were hardly detected in non- nuclear fractions in control or in Dyn. K4. 4A- expressing cells; Fig. S1. B). " [Show abstract][Hide abstract]ABSTRACT: Activation of AP- 1 transcription factors, composed of the Jun and Fos proteins, regulates cellular fates, such as proliferation, differentiation or apoptosis. Among other stimuli, the AP- 1 pathway can be initiated by extracellular ligands, such as growth factors or cytokines, which undergo internalization in complex with their receptors. Endocytosis has been implicated in the regulation of several signaling pathways; however its possible impact on AP- 1 signaling remains unknown. Here we show that inhibition of dynamin 2 (Dyn. AP- 1 pathway. Specifically, expression of a dominant- negative Dyn.
K4. 4A mutant increases the total levels of c- Jun, its phosphorylation on Ser. AP- 1 target genes. Interestingly, DNM2 mutations implicated in human neurological disorders exhibit similar effects on AP- 1 signaling.
Mechanistically, Dyn. K4. 4A induces AP- 1 by increasing phosphorylation of several receptor tyrosine kinases. Their activation is required to initiate a Src- and JNK- dependent signaling cascade converging on c- Jun and stimulating expression of AP- 1 target genes.
Cumulatively, our data uncover a link between the Dyn. JNK signaling which leads to AP- 1 induction. Full- text · Article · Oct 2. Cellular Signalling Show more.
Function and regulation of AP- 1 subunits in skin physiology and pathology. The mouse skin has become the model of choice to study the regulation and function of AP- 1 subunits in many physiological and pathological processes in vivo and in vitro.
Genetically modified mice, in vitro reconstituted skin equivalents and epidermal cell lines were established, in which AP- 1- regulated genetic programs of cell proliferation, differentiation and tumorigenesis can be analysed. Since the epidermis, as our interface with the environment, is subjected to radiation and injury, signal transduction pathways and critical AP- 1 members regulating the mammalian stress response could be identified. Regulated expression of important components of the cytokine network, cell surface receptors and proteases, which orchestrate the process of wound healing has been found to rely on AP- 1 activity. Here we review our current knowledge on the function of AP- 1 subunits and AP- 1 target genes in these fascinating fields of skin physiology and pathology. Oncogene (2. 00. 1) 2.