| Name | H ras |
|---|---|
| Synonyms | C H RAS; Transforming protein p21; N ras; HRAS1; HRASP; C H ras 1 protein N terminal fragment (37 AA); C has/bas p21 protein; C ras Ki 2 protein… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12016150 | Okoji RS, Yu RC, Maronpot RR, Froines JR: Sodium arsenite administration via drinking water increases genome-wide and Ha-ras DNA hypomethylation in methyl-deficient C57BL/6J mice. Carcinogenesis. 2002 May;23(5):777-85. This study sought to determine the role of a methyl-deficient diet in combination with sodium arsenite on the genomic methylation status and Ha-ras methylation status of C57BL/6J male mice hepatic DNA. |
171(2,2,3,6) | Details |
| 15345372 | Xie Y, Trouba KJ, Liu J, Waalkes MP, Germolec DR: Biokinetics and subchronic toxic effects of oral arsenite, arsenate, monomethylarsonic acid, and dimethylarsinic acid in v-Ha-ras transgenic (Tg.AC) mice. Environ Health Perspect. 2004 Aug;112(12):1255-63. Previous research demonstrated that 12-O-tetradecanoylphorbol-13- (TPA) treatment increased the number of skin papillomas in v-Ha-ras transgenic (Tg.AC) mice that had received sodium arsenite [(As (III)] in drinking water, indicating that this model is useful for studying the toxic effects of arsenic in vivo. |
7(0,0,1,2) | Details |
| 16039940 | Benbrahim-Tallaa L, Waterland RA, Styblo M, Achanzar WE, Webber MM, Waalkes MP: Molecular events associated with arsenic-induced malignant transformation of human prostatic epithelial cells: aberrant genomic DNA methylation and K-ras oncogene activation. Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98. Epub 2005 Jan 18. Our prior work showed that chronic arsenic exposure of the non-tumorigenic, human prostate epithelial cell line, RWPE-1, to low levels of (5 microM) sodium arsenite for 29 weeks resulted in malignant transformation and produced the tumorigenic CAsE-PE cell line. |
6(0,0,0,6) | Details |
| 9219559 | Germolec DR, Spalding J, Boorman GA, Wilmer JL, Yoshida T, Simeonova PP, Bruccoleri A, Kayama F, Gaido K, Tennant R, Burleson F, Dong W, Lang RW, Luster MI: Arsenic can mediate skin neoplasia by chronic stimulation of keratinocyte-derived growth factors. Mutat Res. 1997 Jun;386(3):209-18. We observed increased mRNA transcripts and secretion of keratinocyte growth factors, including granulocyte macrophage-colony stimulating factor (GM-CSF) and transforming growth factor-alpha (TGF-alpha) and the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in primary human epidermal keratinocytes cultured in the presence of low micromolar concentrations of sodium arsenite. As an in vivo model, the influence of arsenic on mouse skin tumor development was studied in transgenic TG.AC mice which carry the v-Ha-ras oncogene, and can serve as a genetically initiated model for skin carcinogenesis. |
1(0,0,0,1) | Details |
| 15590121 | Hernandez-Zavala A, Cordova E, Del Razo LM, Cebrian ME, Garrido E: Effects of arsenite on cell cycle progression in a human bladder cancer cell line. Toxicology. 2005 Feb 1;207(1):49-57. Experimental studies have shown that As exposure induces cell proliferation in the bladder of sodium arsenite (iAsIII) subchronically treated mice. The time-course of iAsIII effects (10 microM) showed an increase in p53 protein content and a transient increase in p21 protein levels accompanying the changes in S-phase. |
1(0,0,0,1) | Details |
| 12115494 | Takahashi M, Barrett JC, Tsutsui T: Transformation by inorganic arsenic compounds of normal Syrian hamster embryo cells into a neoplastic state in which they become anchorage-independent and cause tumors in newborn hamsters. Int J Cancer. 2002 Jun 10;99(5):629-34. Amplification of the c-myc or c-Ha-ras oncogene was detected in 3 of 5 and 4 of 5 tumorigenic cell lines, respectively. In order to investigate the ability of inorganic arsenics to transform normal cells into a neoplastic state, mass cultures of normal, diploid Syrian hamster embryo (SHE) cells exposed to various concentrations of sodium arsenite or arsenate for 48 hr were continually passaged and tested for neoplastic transformation, as determined by anchorage-independent growth in semisolid agar and tumorigenicity in newborn hamsters. |
1(0,0,0,1) | Details |
| 2484630 | Saffiotti U, Bertolero F: Neoplastic transformation of BALB/3T3 cells by metals and the quest for induction of a metastatic phenotype. Biol Trace Elem Res. 1989 Jul-Sep;21:475-82. Metastatic and type IV collagenolytic activities can be induced by transfection of the c-Ha-ras oncogene and inhibited by the Ad2-E1a gene (so far shown in other cell types). |
1(0,0,0,1) | Details |
| 2113536 | Nakai A, Hirayama C, Ohtsuka K, Hirayoshi K, Nagata K: Novel ATP-binding heat-inducible protein of Mr = 37,000 that is sensitive to transformation in BALB/3T3 cells. J Cell Physiol. 1990 Jun;143(3):577-89. The synthesis and the total amount of this ATP-binding protein increased in mouse 3T3 cells transformed by simian virus 40, methylcholanthrene, or activated c-Ha-ras oncogene compared to their normal counterparts. This protein was drastically induced by treating the cells with alpha,alpha'-dipyridyl, an iron chelating reagent, but not with sodium arsenite, ionophore, or tunicamycin. |
1(0,0,0,1) | Details |
| 19386250 | Muramatsu D, Sasaki K, Kuroda S, Hayashi K, Tanaka N, Sakai A: Comparison of sensitivity to arsenic compounds between a Bhas 42 cell transformation assay and a BALB/c 3T3 cell transformation assay. Mutat Res. 2009 Apr 30;675(1-2):66-70. Epub 2009 Feb 28. A short-term cell transformation assay has recently been developed, using Bhas 42 cells which were established from BALB/c 3T3 cells transfected by v-Ha-ras gene and postulated to be initiated in the two-stage carcinogenesis theory. Sodium arsenite, disodium arsenate, and their metabolites, monomethylarsonic acid and dimethylarsinic acid (DMAA) were included in the study. |
1(0,0,0,1) | Details |
| 18037969 | Wen G, Calaf GM, Partridge MA, Echiburu-Chau C, Zhao Y, Huang S, Chai Y, Li B, Hu B, Hei TK: Neoplastic transformation of human small airway epithelial cells induced by arsenic. Mol Med. 2008 Jan-Feb;14(1-2):2-10. Human small airway epithelial cells (SAECs) previously immortalized with human telomerase reverse transcriptase (h-TERT) were continuously treated with sodium arsenite at a dose of 0.5 microg/mL in culture for up to 6 months. In addition, arsenic-treated cells showed an increase in c-H-ras, c-myc, and c-fos protein expression relative to controls. |
1(0,0,0,1) | Details |
| 8228242 | Tamura Y, Tsuboi N, Sato N, Kikuchi K: 70 kDa heat shock cognate protein is a transformation-associated antigen and a possible target for the host's anti-tumor immunity. J Immunol. 1993 Nov 15;151(10):5516-24. The accumulated data indicated that the cell surface expression of Ag was clearly enhanced by several stressors, such as TNF, L-azetidine-2-carboxylic acid, and sodium arsenite. |
0(0,0,0,0) | Details |
| 9671310 | Doza YN, Hall-Jackson CA, Cohen P: Arsenite blocks growth factor induced activation of the MAP kinase cascade, upstream of Ras and downstream of Grb2-Sos. Oncogene. 1998 Jul 9;17(1):19-24. Pretreatment of cells with 0.5 mM sodium arsenite (but not other activators of stress-activated MAP kinase cascades) prevents the activation of p21Ras and strongly suppresses the activation of c-Raf and the MAP kinase cascade by a variety of growth factors. |
0(0,0,0,0) | Details |