The c-jun gene regulates cellular proliferation and apoptosis via direct regulation of cellular gene expression. Alternative splicing of pre-mRNA increases the diversity of protein functions, and alternate splicing events occur in tumors. Here, by targeting the excision of the endogenous c-jun gene within the mouse mammary epithelium, we have identified its selective role as an inhibitor of RNA splicing. Microarray-based assessment of gene expression, on laser capture microdissected c-jun−/− mammary epithelium, showed that endogenous c-jun regulates the expression of approximately 50 genes governing RNA splicing. In addition, genome-wide splicing arrays showed that endogenous c-jun regulated the alternate exon of approximately 147 genes, and 18% of these were either alternatively spliced in human tumors or involved in apoptosis. Endogenous c-jun also was shown to reduce splicing activity, which required the c-jun dimerization domain. Together, our findings suggest that c-jun directly ...
Heat Shock Protein 90 Regulates the Stability of c-Jun in HEK293 Cells c-Jun;Geldanamycin;Heat Shock Protein 90;HEK293 Cells;Jun-2 Luciferase Reporter;MG132; The 90-kDa heat shock protein (HSP90) normally functions as a molecular chaperone participating in folding and stabilizing newly synthesized proteins, and refolding denatured proteins. The HSP90 inhibitor geldanamycin (GA) occupies the ATP/ADP binding pocket of HSP90 so inhibits its chaperone activity and causes subsequent degradation of HSP90 client proteins by proteasomes. Here we show that GA reduces the level of endogenous c-Jun in human embryonic kidney 293 (HEK293) cells in a time and dose dependent manner, and that this decrease can be reversed by transfection of HSP90 plasmids. Transfection of HSP90 plasmids in the absence of GA increases the level of endogenous c-Jun protein, but has no obvious affect on c-Jun mRNA levels. We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N
Assembled_chromosomes/ 17-Jun-2016 21:20 - CHR_02/ 17-Jun-2016 21:20 - CHR_03/ 17-Jun-2016 21:20 - CHR_04/ 17-Jun-2016 21:20 - CHR_05/ 17-Jun-2016 21:20 - CHR_XL/ 17-Jun-2016 21:20 - CHR_XR/ 17-Jun-2016 21:20 - GFF/ 20-Jun-2016 17:28 - Gnomon/ 26-Jul-2016 21:37 - RNA/ 17-Jun-2016 21:39 - other/ 17-Jun-2016 21:20 - protein/ 17-Jun-2016 21:39 - README 20-Jun-2016 17:26 28921 README_CURRENT_RELEASE 17-Jun-2016 21:21 540 allcontig.agp.gz 17-Jun-2016 21:20 115096 annotation_report.xml 17-Jun-2016 21:03 60953 masking_coordinates.gz 17-Jun-2016 21:20 1960640 scaffold_names 17-Jun-2016 21:20 463 windowmasker_nmer.oascii.gz 17-Jun-2016 21:04 6436878 ...
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To test the hypothesis that the difference in the directions of DNA bending induced by transcription activation domains linked to the bZIP region of Fos versus Jun was due to a preferred orientation of heterodimer binding to the AP‐1 site, we examined bending at additional binding sites. The relative directions of DNA bending induced by the transcription activation domains fused to the Fos versus Jun bZIP domains at the M, X, MX, XM and X6G sites were similar (Figure 5), suggesting that Fos-Jun heterodimers bind to these sites in the same preferred orientation. These AP‐1 sites share an asymmetric central C:G base pair. To examine the influence of this central base pair on the orientation of heterodimer binding and to explore the relationship between binding orientation and DNA bending, we examined DNA bending at two sites that contained a central G:C base pair. One site (W) is identical to the M site with the exception of transversion of the central C:G base pair to a G:C base pair. The ...
Transcription factor involved in regulating gene activity following the primary growth factor response. Binds to the DNA sequence 5-TGA[CG]TCA-3.
Background The c-proto-oncogene is an archetype for rapid and integrative transcriptional activation. central nervous system (CNS) and the mesenchyme of developing mammary buds in embryos 12.5 days post-conception, and to brain tissue in adults. RT-QPCR analysis of tissue mRNA, including the anlage of the mammary gland and the CNS, confirms the presence of a novel, nested mRNA initiated in the first intron. Conclusions/Significance Our results provide evidence for a novel, regulated promoter within the initial intron from the c-gene developmentally. Mmp27 Launch The c-proto-oncogene item, c-Fos, dimerizes with people from the Jun family members to create the transcription aspect AP-1, which regulates several genes in response to numerous stimuli [1]. c-gene activation continues to be researched since it exemplifies the fast thoroughly, transient reaction to extracellular stimuli. c-is held silent generally in most cell types but is certainly robustly induced by way of a wide variety of agencies ...
The goal of this project is to elucidate the mechanisms by which the AP-1 transcription factor JunB regulates normal hematopoiesis, and to understand how loss o...
The buildroot used for fedora 7 updates building is not self updating. It only contains things from f7-gold, and stable released updates. This means that one update candidate cannot be built against another update candidate without rel-eng interaction. We havent been very vocal about this yet, and it isnt documented anywhere ...
c-Jun兔多克隆抗体(ab428)可与鸡, 哺乳动物样本反应并经WB, EMSA实验严格验证,被6篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Looking for online definition of Proto-oncogene c-Jun in the Medical Dictionary? Proto-oncogene c-Jun explanation free. What is Proto-oncogene c-Jun? Meaning of Proto-oncogene c-Jun medical term. What does Proto-oncogene c-Jun mean?
Nerve injury triggers numerous changes in the injured neurons and surrounding nonneuronal cells that ultimately result in successful target reinnervation or cell death. c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is highly expressed in response to neuronal trauma. Here we have investigated the role of c-jun during axonal regeneration using mice lacking c-jun in the central nervous system. After transection of the facial nerve, the absence of c-Jun caused severe defects in several aspects of the axonal response, including perineuronal sprouting, lymphocyte recruitment, and microglial activation. c-Jun-deficient motorneurons were atrophic, resistant to axotomy-induced cell death, and showed reduced target muscle reinnervation. Expression of CD44, galanin, and alpha7beta1 integrin, molecules known to be involved in regeneration, was greatly impaired, suggesting a mechanism for c-Jun-mediated axonal growth. Taken together, our results identify c-Jun as an important ...
Figure 4: TPEN induces activation of NF-κB, p53 and c-Jun transcription factors, caspase-3, and AIF in Jurkat T cells. Jurkat cells (1 × 106 cells/mL) were incubated with TPEN (3 μM) at 37°C for 24 hours. Untreated (a) and TPEN-treated cells were stained with anti-NF-κB-p65 (b), anti-p53 (c), anti-c-Jun (d), anti-caspase-3 (e), and anti-AIF (f) antibodies according to protocol described in according to Material and Methods section Notice that compared to control, NF-κB, p53, c-Jun, caspase-3, and AIF positive nuclei (dark brown color) reflect their nuclear translocation/activation and appear to correlate with the apoptotic nuclear morphology. Notice also that (a) represents the control for each antibody used in ((b)-(f)). Magnification 700x ((a)-(f ...
Given the apparent importance of hypha formation in pathogenicity and epithelial activation, determining how ECs are activated by the yeast and hyphal form of C. albicans is of fundamental importance. To this end, recently a novel mechanism was identified that enables oral ECs to discriminate between C. albicans yeast and hyphae. Oral ECs orchestrate responses to C. albicans via NF-κB and a bi-phasic MAPK signaling response. Activation of NF-κB and an initial, transient MAPK response, resulting in activation of the c-Jun transcription factor, is independent of morphology and thus activated by both yeast and hyphae. However, activation of a second, stronger MAPK response, resulting in activation of the c-Fos transcription factor and production and stabilisation of the MAPK phosphatase MKP1, is specifically associated with hypha formation and correlates with proinflammatory responses and cell damage. A key finding was that the hypha-mediated response was strongly dose-dependent, indicating that ...
Given the apparent importance of hypha formation in pathogenicity and epithelial activation, determining how ECs are activated by the yeast and hyphal form of C. albicans is of fundamental importance. To this end, recently a novel mechanism was identified that enables oral ECs to discriminate between C. albicans yeast and hyphae. Oral ECs orchestrate responses to C. albicans via NF-κB and a bi-phasic MAPK signaling response. Activation of NF-κB and an initial, transient MAPK response, resulting in activation of the c-Jun transcription factor, is independent of morphology and thus activated by both yeast and hyphae. However, activation of a second, stronger MAPK response, resulting in activation of the c-Fos transcription factor and production and stabilisation of the MAPK phosphatase MKP1, is specifically associated with hypha formation and correlates with proinflammatory responses and cell damage. A key finding was that the hypha-mediated response was strongly dose-dependent, indicating that ...
Angiogenesis, the formation of new blood vessels from the existing vasculature, is a prerequisite for the progression of solid tumor growth and metastasis. In this study it is shown that the COP9 signalosome (CSN) regulates the stability of the angiogenic transcription factors c-Jun, Id1 and Id3 towards the ubiquitin/26S proteasome system. The COP9 signalosome constitutes a multimeric protein complex that shares sequence homology with the 26S proteasome lid complex. Both c-Jun and Id3 physically interact with the CSN subunit CSN5. In addition, Id3 can bind to CSN7. Recombinant c-Jun, a substrate of the CSN-associated kinases CK2 und PKD, is destabilized by curcumin, an inhibitor of these two kinases. Furthermore, curcumin induces high molecular weight c-Jun species, most likely ubiquitin conjugates. All tested inhibitors of the CK2 and PKD, emodin, DRB, resveratrol, as well as curcumin accelerate the degradation of c-Jun by the 26S proteasome in HeLa cells. The c-Jun-dependent expression of ...
Angiogenesis, the formation of new blood vessels from the existing vasculature, is a prerequisite for the progression of solid tumor growth and metastasis. In this study it is shown that the COP9 signalosome (CSN) regulates the stability of the angiogenic transcription factors c-Jun, Id1 and Id3 towards the ubiquitin/26S proteasome system. The COP9 signalosome constitutes a multimeric protein complex that shares sequence homology with the 26S proteasome lid complex. Both c-Jun and Id3 physically interact with the CSN subunit CSN5. In addition, Id3 can bind to CSN7. Recombinant c-Jun, a substrate of the CSN-associated kinases CK2 und PKD, is destabilized by curcumin, an inhibitor of these two kinases. Furthermore, curcumin induces high molecular weight c-Jun species, most likely ubiquitin conjugates. All tested inhibitors of the CK2 and PKD, emodin, DRB, resveratrol, as well as curcumin accelerate the degradation of c-Jun by the 26S proteasome in HeLa cells. The c-Jun-dependent expression of ...
Fibronectin (FN) is transactivated by human papillomavirus type 16 (HPV16) E6 via the induction of c-Jun-ATF-2 complexes binding to the cyclic AMP response element (CRE) in the FN promoter. The present study analyzed c-Jun regulation of FN gene expression. Northern and immunoblot analyses showed that c-Jun expression was enhanced in HPV16-E6-expressing cells. However, mouse 10T1/2 cell lines overexpressing c-Jun showed an inverse correlation between the expression levels of c-Jun and those of FN. Luciferase assays indicated that the FN promoter was strongly repressed in c-Jun-overexpressing mouse 10T1/2 cells. Deletion and mutation analyses of the FN promoter revealed that repression of the FN promoter by c-Jun depends on the CRE located at -160 relative to the start site of transcription. Supershift assays of CRE-bound complexes from HPV16-E6-expressing and c-Jun-overexpressing cells suggested that the presence of ATF-2 in the complexes binding to CRE was required for the transactivation of the ...
Transcription factor jun-B is a protein that in humans is encoded by the JUNB gene. Transcription factor jun-B is a transcription factor involved in regulating gene activity following the primary growth factor response. It binds to the DNA sequence 5-TGA[CG]TCA-3. JUNB has been shown to interact with BRCA1, and SMAD3. AP-1 (transcription factor) GRCh38: Ensembl release 89: ENSG00000171223 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000052837 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". Schütte J, Viallet J, Nau M, Segal S, Fedorko J, Minna J (Feb 1990). "jun-B inhibits and c-fos stimulates the transforming and trans-activating activities of c-jun". Cell. 59 (6): 987-997. doi:10.1016/0092-8674(89)90755-1. PMID 2513129. "Entrez Gene: JUNB jun B proto-oncogene". Hu YF, Li R (Jun 2002). "JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction". Genes Dev. 16 (12): 1509-17. doi:10.1101/gad.995502. PMC 186344 ...
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TransAM AP-1 Kits are DNA-binding ELISAs that quantify activated c-Fos, FosB, c-Jun, JunB, JunD & Fra-1 transcription factors using a method that is faster and more sensitive than gelshift, without radioactivity and gels.
Parent Directory - 00index.txt 26-Aug-2003 12:30 12K 2dtoolkit.sit.hqx 04-May-1994 15:12 16K aminoacid.sit.hqx 27-Dec-1990 15:09 94K atoms.sit.hqx 27-Dec-1990 15:09 95K ballandstick3.51demo.., 13-Jun-1993 03:30 279K bands2macmol1.0.cpt.hqx 26-Jun-1993 22:56 48K bonding.sit.hqx 27-Dec-1990 15:10 53K caisciencelessons.si.., 03-Feb-1995 05:05 492K chem3dnet3.2.sea.hqx 10-Nov-1995 22:39 2.7M chemaid1.02b.sit.hqx 05-Sep-1993 22:15 156K chemdrawnet3.51.sea.hqx 10-Nov-1995 22:44 2.0M chemedit.cpt.hqx 27-Aug-1995 04:06 312K chemicalhazards.sit.hqx 04-Feb-1996 08:25 150K chemriddles.sit.hqx 09-Sep-1992 02:33 34K chn1.6.sit.hqx 10-Jun-1997 06:39 39K counterion.cpt.hqx 31-Oct-1994 13:04 83K crystal2.29.cpt.hqx 28-Mar-1994 22:04 155K crystaldiffract1.10..., 04-Feb-1996 18:39 472K crystalmakerdemo1.17.., 08-Dec-1995 02:26 959K crystalview1.0.cpt.hqx 28-Mar-1994 22:04 115K elements.sit.hqx 27-Dec-1990 15:15 119K elementtwo.hqx 27-Dec-1990 15:15 65K evtransmogrifier2.0..., 25-Sep-1994 07:31 44K ...
上海-许多人对中国经济的增长前景感到十分悲观,因为大规模债务、过度投资、产能过剩以及2008年全球金融危机以来的所谓"鬼城"逐渐出现。但这些问题都不是新问题。自1978年以来,它们就以各种方式影响着中国经济,东亚的其他高增长经济体--台湾、韩国甚至日本--在快速增长时期也无不遇到过这些问题。. 尽管如此,自邓小平启动他的"改革开放"政策以来,中国平均年增长率高达9.7%。而韩国和台湾都只花了40年时间完成了从低收入到高收入的转型。. 这些经济提是如何成功地以如此快速增长如此长时间,并克服期间所面临的严重问题的?答案很简单:恢复力(resilience)。 ...
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The c-Fos and c-Jun transcription factors are rapidly turned over in vivo. One of the multiple pathways responsible for their breakdown is probably initiated by calpains, which are cytoplasmic calcium-dependent cysteine proteases. The c-fos gene has been transduced by two murine oncogenic retroviruses called Finkel-Biskis-Jenkins murine sarcoma virus (FBJ-MSV) and Finkel-Biskis-Reilly murine sarcoma virus (FBR-MSV); c-jun has been transduced by the chicken avian sarcoma virus 17 (ASV17) retrovirus. Using an in vitro degradation assay, we show that the mutated v-FosFBR, but not v-FosFBJ or v-JunASV17, is resistant to calpains. This property raises the interesting possibility that decreased sensitivity to calpains might contribute to the tumorigenic potential of FBR-MSV by allowing greater accumulation of the protein that it encodes in infected cells. It has also been demonstrated that resistance to cleavage by calpains does not result from mutations that have accumulated in the Fos moiety of the ...
yfworgh_b.htm Oregon Institute of Technology December 18, 2017 Organization Hierarchy Report 06:15 Both Active And Inactive Codes Data Effective Termination Next Change Organization Code Title Entry Status Date Date Date ---------------------- ------------------------------------ ----- ------ ----------- ----------- ----------- 000000 Oregon Institute of Technology N A 01-JUL-1993 31-DEC-2099 000500 President N A 25-JUN-2011 31-DEC-2099 000503 Presidents Operations N A 01-JUL-2015 31-DEC-2099 000505 Presidents Office Y A 01-JUL-2015 31-DEC-2099 000512 Dues & Memberships Y I 05-JUN-2016 05-JUN-2016 31-DEC-2099 000515 Councils Boards Commissions Y I 25-JUN-2016 25-JUN-2016 31-DEC-2099 000530 Title III Project Y I 04-JUN-2016 04-JUN-2016 31-DEC-2099 000534 Renewable Energy Study Trip (ETIC) Y A 01-JUL-2015 31-DEC-2099 000540 Title IX Program Y A 01-JUL-2016 31-DEC-2099 000600 Oregon Technology Center N I 27-OCT-2016 27-OCT-2016 31-DEC-2099 000601 OTC Contract Training N I 30-OCT-2008 30-OCT-2008 ...
Cells. Mouse melanoma (SW1) and human melanoma (LU1205) cells were maintained in DMEM supplemented with 10% fetal bovine serum, l-glutamine, and antibiotics. The human melanoma cell lines MEWO and WM115 were maintained in RPMI 1640 supplemented with 10% fetal bovine serum and antibiotics. Primary mouse melanocytes were cultured in F-12 medium supplemented with 10% fetal bovine serum, antibiotics, isobutylmethylxanthine, bovine pituitary extract, and 12-O-tetradecanoylphorbol-13-acetate.. Constructs and inhibitors. An ATF2 peptide (amino acids 51-100) was cloned into HA-tagged pcDNA3 vector as described previously (30). 5xJun2tk-Luc (marker for ATF2 transcriptional activities), 5xTRE-tk-Luc (marker for AP1/c-Jun transcriptional activities), and 2xNF-κB-Luc were described previously (31). Pharmacologic inhibitor of JNK (SP600125) was purchased (EMD Biosciences) and added (5 μmol/L) to cultured cells as indicated in Results.. Transcriptional analysis. Transient transfection of different reporter ...
Members of the AP‐1 transcription complex were shown to be important regulators of the G0-G1 transition of the cell cycle. In the present study, we investigated the role of some of these genes in normally cycling cells. Combining flow cytometry measurements, immunofluorescence staining and Western blotting experiments, we showed that c‐Jun protein levels varied little during the cell cycle. In contrast, JunB displayed a highly heterogeneous distribution, especially in the G2/M and G1 phases. Immuno fluorescence microscopy revealed that the level of JunB protein was low in mitotic cells. Using synchronized cells, we were able to define more precisely the timing of the decrease in JunB abundance and showed that it was correlated with an increase in its apparent molecular weight, due to phosphorylation.. We investigated which kinase may be responsible for JunB phoshorylation. JunB contains a JNK docking site, but lacks serine residues analogous to the phosphorylated sites in c‐Jun. While ...
Lee, J.Hee.; Ko, H.Ju.; Woo, E-Rhan.; Lee, S.Kook.; Moon, B.Soo.; Lee, C.Woo.; Mandava, S.; Samala, M.; Lee, J.; Kim, H.Pyo., 2016: Moracin M inhibits airway inflammation by interrupting the JNK/c-Jun and NF-κB pathways in vitro and in vivo
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The epidermal growth factor receptor (EGFR) family regulates essential natural processes. and function of Elk-1 recruiting it towards the TBP promoter. On the other hand EGFRvIII robustly induces c-jun appearance rousing recruitment of c-fos/c-jun for an overlapping AP-1 site. Improving c-jun appearance by itself induces TBP promoter activity through the AP-1 site. To look for […]. ...
O level specimen paper 2010 english - thebookshq.com where can i find specimen papers for gce as level biology 2009. Unit 1: specimen question paper o level biology edexcel specimen :: provided by freeexampapers which is a provider of free past papers for different education levels. O level biology (7040) mark scheme for specimen papers paper 1 cambridge international examinations o-level past paper order form ordering examinations subject/ code paper no jun-07 nov-2007 jun-2008 nov-2008 jun-2009 nov-2009 biology paper. Igcse - biology - flying colours o level biology 5090: the syllabus offers a combination of theoretical and practical specimen papers and mark schemes download pdf examination paper - foundation tier. Free English Essays. ...
The epidermal growth factor receptor (EGFR) family regulates essential natural processes. and function of Elk-1 recruiting it towards the TBP promoter. On the other hand EGFRvIII robustly induces c-jun appearance rousing recruitment of c-fos/c-jun for an overlapping AP-1 site. Improving c-jun appearance by itself induces TBP promoter activity through the AP-1 site. To look for […]. ...
The coding sequences of murine c-jun, junB, or junD, which code for proteins with practically identical dimerization and DNA binding properties, were
Order C-JUN ELISA Kits for many Reactivities. Chicken, Cow, Dog and more. Compare C-JUN ELISA Kits and find the right product on antibodies-online.com.
The Juan Rosai Collection of Pathology Slides, a comprehensive collection of slide seminars including histopathology slides of rare and educational pathological cases
Jika Hidup ini seumpama rel kereta api dalam eksperimen relativitas, maka pengalaman demi pengalaman yang mengempur kita dari waktu ke waktu adalah cahaya yang melesat-lesat di dalam gerebong di atas rel itu. Relativitasnya berupa seberapa banyak kita dapat mengambil pelajaran dari pengalaman yang melesat-lesat itu, maka analoginya adalah jika pengalaman yang sama dapat menimpa siapa saja, namun sejauh mana dan secepat apa pengalaman itu memberi pelajaran pada seseorang, hasilnya akan berbeda, relatif satu sama lain ...
There is no place for the return to barbarism of The Justinian Code to be found as the foundation of the EUs laws where everything is the gift of the State under license when we have 800 years ago renounced the Corpus Juris of the EU in favour of the Universal Rights of Mankind as enshrined in the Magna Carta where the people hold the rights and the state and its various goffers are the servants of the people ...
Nesprin-2 mediates the translocation of c-Fos after TGFβ induction. (A) Nuclear translocation of transcription factor c-Fos was studied in control and KD HaCaT
Jun Li: A note on the null-additivity of the fuzzy measure: Corrigendum to "On the null-additivity of the fuzzy measure" [Fuzzy Sets and Systems 78 (1996) 337-339]. Fuzzy Sets and Systems 125(2): 269-271 (2002 ...
c-Fos兔多克隆抗体(ab429)可与鸡样本反应并经WB, EMSA实验严格验证,被6篇文献引用并得到1个独立的用户反馈。所有产品均提供质保服务,中国75%以上现货。
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TY - JOUR. T1 - CD14- and toll-like receptor 4-dependent regulation of c-Fos, c-Jun and c-Jun phosphorylation in the adrenal gland after burn injury. AU - Cho, Kiho. AU - Crivello, Sicily D.. AU - Vanhook, Tajia G.. AU - Greenhalgh, David G.. PY - 2004. Y1 - 2004. N2 - Objectives: Although the pathophysiology of the adrenocortical response after injury has been described, alterations in the molecular profile (e.g. transcription factors) of the adrenal gland itself are not well understood. The regulation of c-Fos, c-Jun, and c-Jun phosphorylation in the adrenal gland after burn injury was investigated in this study. In addition, since burn injury is often associated with lipopolysaccharide (LPS)-mediated sepsis, we examined the involvement of the LPS signaling pathway in the regulation of these transcription factors utilizing CD14 knockout and C3H/HeJ (encoding defective toll-like receptor 4) mice. Methods: Adrenal glands harvested after an 18% total body surface area burn were subjected to ...
In this study, we demonstrated a set of novel clinical and molecular mechanistic findings: (a) MELK protein is elevated in HGGs and GSCs derived from these tumors; (b) MELK immunoreactivity is a prognostic indicator of the postsurgical survival periods of HGG patients; (c) MELK is required for the growth of GSCs both in vitro and in vivo; (d) the JNK/c-JUN pathway regulates nuclear MELK in GSCs, but not in normal cells; (e) c-JUN physically associates with MELK, and this protein complex formation is dependent on the kinase activity of MELK; (f) p53 and MELK expressions in GBM cells are mutually exclusive and p53 negatively regulates MELK action on GSCs; (g) radiation treatment increases the expression of MELK and c-JUN in GSCs in vitro and in vivo; and (h) the expression of MELK is elevated in relapsed and recurrent GBM tumors compared with untreated GBM tumors. Therefore, the JNK-driven c-JUN/MELK interaction represents a critical mechanism for controlling GSC survival, self-renewal, ...
Heparin is a potent inhibitor of the proliferation and migration of vascular smooth muscle cells. This agent selectively inhibits the transcription of tissue-type plasminogen activator and interstitial collagenase, probably by decreasing the binding of activator protein-1 (AP-1) to phorbol ester-responsive elements in the promoters of these genes. Decreased AP-1 binding is not due to a direct inhibition by heparin, since heparinase digestion of nuclear extracts prepared from heparin-treated smooth muscle cells does not restore AP-1 binding activity. Treatment of cells with heparin suppresses the expression of Jun B, one of the components of AP-1. The major effect of heparin is at the level of posttranslational modification of Jun B. Results from pulse-chase labeling experiments show that the newly synthesized Jun B is rapidly converted to a higher-molecular-weight form and that conversion is suppressed by heparin. Evidence is presented suggesting that the heparin-inhibited event is ...
c-Jun is a member of the early mammalian transcriptional regulators belonging to the AP-1 family, which participates in a wide range of cellular processes such as proliferation, apoptosis, tumorigenesis, and differentiation. Despite its established role in cell survival upon stress, its participation in the stress response induced by bacterial infections has been poorly investigated. To study the potential role of c-Jun in this context we choose the widely studied α-toxin produced by Staphylococcus aureus, a pore-forming toxin that is a critical virulence factor in the pathogenesis of these bacteria. We analyzed the effect of α-toxin treatment in the activation, expression, and protein levels of c-Jun in A549 lung epithelial cells. Furthermore, we explored the role of c-Jun in the cellular fate after exposure to α-toxin. Our results show that staphylococcal α-toxin per se is able to activate c-Jun by inducing phosphorylation of its Serine 73 residue. Silencing of the JNK (c-Jun N-terminal Kinase)
De Felipe, C. and Belmonte, C. (1999), c-Jun expression after axotomy of corneal trigeminal ganglion neurons is dependent on the site of injury. European Journal of Neuroscience, 11: 899-906. doi: 10.1046/j.1460-9568.1999.00498.x ...
c-Jun enhancement of cyclic adenosine 3,5-monophosphate response element-dependent transcription induced by transforming growth factor-beta is independent of c-Jun binding to DNA.