Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: UNIPROT:O76050 (
neu
)
3,969
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Transformation of NIH3T3 cells with the ras, the sis, or the
neu
oncogene rendered cells less susceptible to cis-diamminedichloroplatinum(II). Since resistance to cis-diamminedichloroplatinum(II) is reported to be associated with increased levels of metallothionein, we examined effects of these oncogenes on metallothionein gene expression. NIH3T3 cells were first transfected with the lacZ gene whose transcription is under the control of mouse metallothionein I promoter and then with the ras, the sis, or the
neu
oncogene. The ras and the sis oncogenes increased beta-galactosidase activities which were induced either by metal (
cadmium
and zinc) or by glucocorticoid (dexamethasone), whereas the
neu
oncogene repressed its activity. When SV40 early promoter was used instead of metallothionein I promoter for the lacZ gene transcription, the beta-galactosidase activities were not affected by metal, dexamethasone, or any of these oncogenes. This result was coincident with that of reverse transcription polymerase chain reaction that metal-induced MT I mRNA was only detected in the sis- or the ras-transformed cells, whereas any of these oncogenes did not affect the metal-induced transcription of the MT II gene. These results demonstrate that the ras and the sis oncogenes upregulate the metal- or glucocorticoid-induced transcription from metallothionein I promoter, but the
neu
oncogene negatively regulates it. Thus, resistance to the chemotherapeutic agent by oncogenic transformation is partly associated with the metallothionein gene expression, and MT I and MT II gene expressions are differently controlled by different oncogenes.
...
PMID:Effects of oncogenes on the resistance to cis-diamminedichloroplatinum(II) and metallothionein gene expression. 764 18
The effects of aqueous extract of
Schizandra Chinensis Fruit
(AESC) on
cadmium
-induced changes of monoamine neurotransmitters in the different brain regions of adult rats were investigated. Male rats were received intraperitoneal (i.p.) administration of CdCl
2
(0.6 mg/kg/d) for 21 days and sacrificed 7 days after the last administration. Concentrations of norepinephrine (NE), dopamine (DA) in striatum and serotonin (5-HT), 5-hydroxyindole acetic acid (5-HIAA) in cortex were measured by HPLC. There were significant decreases of NE, DA, 5-HT and 5-HIAA in Cd intoxicated rats (
P
< 0.05), while pretreatment with AESC (20 mg/kg/d or 60 mg/kg/d, p.o., 30 min before CdCl
2
) greatly inhibited the decrease of monoamine transmitters, respectively (
P
< 0.05). Also, AESC significantly increased the reduction of glutathione contents and superoxide dismutase activities in cortex induced by CdCl
2
. These results suggest that AESC ameliorates Cd-induced depletion of monoamine
neu
-rotransmitters in brain through its antioxidant activity.
...
PMID:Effects of Aqueous Extract of
Schizandra Chinensis Fruit
on Cadmium-Induced Change of Monoamine Neurotransmitters in Rats. 3203 14
