Abstract:
:Arsenate and arsenite activate c-Jun N-terminal kinase (JNK), however, the mechanism by which this occurs is not known. By expressing inhibitory mutant small GTP-binding proteins, p21-activated kinase (PAK) and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinases (MEKKs), we have identified specific proteins that are involved in arsenate- and arsenite-mediated activation of JNK. We observe a distinct difference between arsenate and arsenite signaling, which demonstrates that arsenate and arsenite are capable of activating unique proteins. Both arsenate and arsenite activation of JNK requires Rac and Rho. Neither arsenate nor arsenite signaling was inhibited by a dominant-negative mutant of Cdc42 or Ras. Arsenite stimulation of JNK requires PAK, whereas arsenate-mediated activation of JNK was unaffected by inhibitory mutant PAK. Of the four MEKKs tested, only MEKK3 and MEKK4 are involved in arsenate-mediated activation of JNK. In contrast, arsenite-mediated JNK activation requires MEKK2, MEKK3 and MEKK4. These results better define the mechanisms by which arsenate and arsenite activate JNK and demonstrate differences in the regulation of signal transduction pathways by these inorganic arsenic species.
journal_name
Oncogenejournal_title
Oncogeneauthors
Porter AC,Fanger GR,Vaillancourt RRdoi
10.1038/sj.onc.1203214subject
Has Abstractpub_date
1999-12-16 00:00:00pages
7794-802issue
54eissn
0950-9232issn
1476-5594journal_volume
18pub_type
杂志文章相关文献
ONCOGENE文献大全abstract::Targeted therapeutics are potential therapeutic agents because of their selectivity and efficacy against tumors resistant to conventional therapy. The goal of this study was to determine the comparative activity of monovalent, engineered anti-Her2/neu immunotoxins fused to recombinant gelonin (rGel) to the activity of...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2012.612
更新日期:2014-01-23 00:00:00
abstract::Acute myeloid leukemia (AML) is a heterogeneous disease comprising a large number of subtypes defined by specific chromosome abnormalities. One such subtype carries the t(6;9)(p22;q34) chromosome rearrangement, which leads to expression of the DEK-NUP214 chimeric gene, and has a particularly poor outcome. To provide a...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2016.118
更新日期:2016-10-27 00:00:00
abstract::As leukemic transformation of myeloproliferative neoplasms (MPNs) worsens the clinical outcome, reducing the inherent risk of the critical event in MPN cases could be beneficial. Among genetic alterations concerning the transformation, the frequent one is TP53 mutation. Here we show that retroviral overexpression of J...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2016.478
更新日期:2017-06-08 00:00:00
abstract::Mutations in p53 change the sensitivity to cancer chemotherapeutic drugs. Whereas many drugs, including the vinca alkaloids, often become less effective when p53 is transcriptionally inactivated, several, most notably paclitaxel, may become more effective. In studying the underlying mechanism(s), we found that increas...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1201658
更新日期:1998-03-26 00:00:00
abstract::A proportion of familial breast cancer has recently been shown by genetic linkage analysis to map to chromosome l3q12 (Wooster et al, 1994). This locus contains a tumor suppressor gene BRCA2, mutations in which lead to tumorigenesis. Genetic alterations at this locus have also been shown in pancreatic adenocarcinoma a...
journal_title:Oncogene
pub_type:
doi:
更新日期:1996-07-04 00:00:00
abstract::To study the interplay of steroid hormones and oncogenes in the control of endometrial cell proliferation and differentiation we have generated cell lines derived from rat endometrium by expressing the immortalizing oncogenes adeno E1A or SV40 large T antigen. These lines are positive for mesenchymal markers and conta...
journal_title:Oncogene
pub_type: 杂志文章
doi:
更新日期:1993-08-01 00:00:00
abstract::The membrane-anchored MMP-regulator RECK is down regulated in many solid tumors; the extent of RECK down regulation correlates with poor prognosis. Forced expression of RECK in tumor cells results in suppression of angiogenesis, invasion, and metastasis. Studies on the roles and the mechanisms of regulation of the REC...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1208733
更新日期:2005-09-01 00:00:00
abstract::Hox gene products, initially characterized as master regulators of embryonic patterning, are also required for proper functioning of adult tissues. There is also a growing body of evidence that links Hox proteins to regulation of cellular proliferation/transformation. However, the underlying molecular mechanisms of Ho...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1203897
更新日期:2000-10-26 00:00:00
abstract::A dual role of transforming growth factor β (TGF-β), to both suppress and promote tumor progression and metastasis, has been well established, but its molecular basis has remained elusive. In this review, we focus on Smad proteins, which are central mediators of the signal transduction of TGF-β family members. We desc...
journal_title:Oncogene
pub_type: 杂志文章,评审
doi:10.1038/onc.2012.191
更新日期:2013-03-28 00:00:00
abstract::Proliferating cell nuclear antigen (PCNA) plays an essential role in nucleic acid metabolism as a component of the replication and repair machinery. This toroidal-shaped protein encircles DNA and can slide bidirectionally along the duplex. One of the well-established functions for PCNA is its role as the processivity ...
journal_title:Oncogene
pub_type: 杂志文章,评审
doi:10.1038/sj.onc.1200886
更新日期:1997-02-13 00:00:00
abstract::Integrins are adhesion receptors that mediate both cell-extracellular matrix and cell-cell interactions. It has also been reported that the loss of integrin alpha4 expression might be associated with metastasis in several cancers. However, the molecular mechanism for loss of their expression in cancers has not been ex...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1207470
更新日期:2004-04-22 00:00:00
abstract::A large body of physiological evidence shows that either upregulation or downregulation of intracellular c-Myc activity has profound consequences on cell cycle progression. Recent work suggests that c-Myc may stimulate the activity of cyclin E/cyclin-dependent kinase 2 (Cdk2) complexes and antagonize the action of the...
journal_title:Oncogene
pub_type: 杂志文章,评审
doi:10.1038/sj.onc.1202749
更新日期:1999-05-13 00:00:00
abstract::The tumor suppressor p53 transcriptionally regulates a large number of target genes that may affect cell growth and cell death pathways. To better understand the role of p53 loss in tumorigenesis, we have developed a mouse mammary cancer model, the Wnt-1 TG/p53 model. Wnt-1 transgenic females that are p53-/- develop m...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1203993
更新日期:2000-12-07 00:00:00
abstract::Rapamycin, a natural product inhibitor of the Raptor-mammalian target of rapamycin complex (mTORC1), is known to induce Protein kinase B (Akt/PKB) Ser-473 phosphorylation in a subset of human cancer cell lines through inactivation of S6K1, stabilization of insulin receptor substrate (IRS)-1, and increased signaling th...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1210343
更新日期:2007-08-16 00:00:00
abstract::MicroRNAs (miRNAs) as modulators of gene expression have been described to display both tumor-promoting and tumor-suppressive functions. Although their role has been studied in different tumor types, little is known about how they regulate nuclear factor κB (NF-κB) signaling in breast cancer. Here, we performed an unb...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2011.571
更新日期:2012-09-13 00:00:00
abstract::Hedgehog pathway activity has been demonstrated in malignant glioma. However, its role in tumor growth has not been determined. Here we demonstrate that pharmacological inhibition of the Hedgehog pathway in established orthotopic malignant glioma xenografts confers a survival advantage. Pathway inhibition is measured ...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2009.208
更新日期:2009-10-01 00:00:00
abstract::The c-myc oncogene is the most extensively studied member of the myc gene family which now consists of three characterized members, namely the c-myc, N-myc and L-myc genes. These genes are often found amplified in cell lines from small cell carcinomas of the lung (SCLC). In this study the L-myc gene was examined in a ...
journal_title:Oncogene
pub_type: 杂志文章
doi:
更新日期:1987-01-01 00:00:00
abstract::A selective switch from expression of Shc1 gene to Shc3 occurs with maturation of neuronal precursors into postmitotic neurons. Previous studies showed that in the embryo, Shc1 is maximally expressed in dividing CNS stem cells while it is silenced in mature neurons, where it is replaced by Shc3. Under normal condition...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1208708
更新日期:2005-08-04 00:00:00
abstract::The DNA-binding, transcriptional activation and transforming activities of the Myc protein require dimerization with Max. Max can form also homodimers which are able to bind the same DNA sequence as Myc/Max heterodimers and suppress Myc-induced transcription and transformation. We have recently identified a naturally ...
journal_title:Oncogene
pub_type: 杂志文章
doi:
更新日期:1995-08-03 00:00:00
abstract::Excessive adiposity has long been associated with increased incidence of breast cancer in post-menopausal women, and with increased mortality from breast cancer, regardless of the menopausal status. Although adipose tissue-derived estrogen contributes to obesity-associated risk for estrogen receptor (ER)-positive brea...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2009.130
更新日期:2009-07-30 00:00:00
abstract::The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance. PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias. Moreover, Friend virus-induced eryth...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1211004
更新日期:2008-05-29 00:00:00
abstract::We have used two different, but complementary assays to characterize functions of SV40 T antigen that are necessary for its ability to immortalize rat embryo fibroblasts. In accordance with previous work, we found that several functions were required. These include activities that map to the p53 binding domain and the...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1203154
更新日期:1999-12-02 00:00:00
abstract::We have optimized the conditions for efficient NIH3T3 focus formation by calcium phosphate transfection of proviral Abelson-murine leukemia virus (A-MuLV) plasmid DNA. Linearized pA-MuLV, P120 or P160 strains, when transfected with calf thymus carrier DNA, will produce 40-50 foci/100 ng pA-MuLV without co-transfecting...
journal_title:Oncogene
pub_type: 杂志文章
doi:
更新日期:1989-11-01 00:00:00
abstract::The cysteine protease cathepsin B (CTSB) is frequently overexpressed in human breast cancer and correlated with a poor prognosis. Genetic deficiency or pharmacological inhibition of CTSB attenuates tumor growth, invasion and metastasis in mouse models of human cancers. CTSB is expressed in both cancer cells and cells ...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/onc.2013.395
更新日期:2014-09-04 00:00:00
abstract::The E3 region of adenovirus induces down-regulation of epidermal growth factor receptor (EGFR) through endocytosis. Here we report that an EGFR-related protein, the HER-2/c-erbB-2 gene product, p185, is also down-regulated by adenovirus, but via a different mechanism. We found that the adenovirus E1a gene is responsib...
journal_title:Oncogene
pub_type: 杂志文章
doi:
更新日期:1991-02-01 00:00:00
abstract::The C3H/HeJ (C3H), A/J and BALB/cByJ (BALB) mouse strains are respectively resistant, sensitive and intermediate regarding the induction of lung tumors by urethane. The phenotypic difference between C3H and A/J is largely determined by the Pas1 (Pulmonary adenoma susceptibility 1) gene on chromosome 6, the A/J allele ...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1201357
更新日期:1997-10-09 00:00:00
abstract::Ras is a major signaling molecule activated by interleukin-6. There have been no published reports, however, that specifically examine the kinetics and percentage of Ras activation in response to IL-6. Model cell lines were used to study activation of N- and K-ras induced by IL-6. All of the myeloma cell lines we test...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1205387
更新日期:2002-12-12 00:00:00
abstract::The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cyto...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1207594
更新日期:2004-06-03 00:00:00
abstract::RasGRP1 is a Ras-specific exchange factor, which is activated by T-cell receptor (TCR) and promotes TCR-dependent positive selection of thymocytes. RasGRP1 is highly expressed on most T lymphocytic leukemias and is a common site of proviral insertion in retrovirus-induced murine T-cell lymphomas. We used RasGRP1 trans...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1208334
更新日期:2005-04-14 00:00:00
abstract::Tumor necrosis factor alpha (TNF alpha) is a proinflammatory cytokine with important roles in regulating inflammatory responses as well as cell cycle proliferation and apoptosis. Although TNFalpha stimulates apoptosis, it also activates the transcription factor NF-kappa B, and studies have shown that inhibition of NF-...
journal_title:Oncogene
pub_type: 杂志文章
doi:10.1038/sj.onc.1206262
更新日期:2003-04-03 00:00:00