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MT3 is an arsenic- and hypoxia-upregulated oncogene that promotes cell growth and invasion of bladder carcinoma cells via downregulation of NDRG1, NDRG2, and MASPIN expressions.
This study suggest that MT3 gene polymorphisms are not associated with autism.
In recent years, the roles of zinc dynamics and MT3 function in neurodegeneration are slowly emerging. This short review focuses on the recent developments regarding the chemistry and biology of MT3. [review]
C-terminal domain of MT3 confers dome formation in MCF-7 cells and the presence of this domain induces expression of the GAGE family of genes. The differential effects of MT3 and metallothionein 1E on the expression of GAGE genes suggests unique roles of these genes in the development and progression of breast cancer.
The expression of MT-3 mRNA in breast cancer cell lines was significantly lower than in the normal human breast epithelial cell line. The results suggest that MT-3 may play a role in the malignant transformation of breast epithelial cells and in tumor progression.
The epidermis of human skin and resulting malignancies express high level of MT-3.
The present study was undertaken to explore further the interrelationship between p53 and metallothioneins.
The study implicates the unique C-terminal sequence of MT-3 in the conversion of HK-2 cells to display an enhanced epithelial phenotype.
MT3 may regulate breast cancer cell invasiveness by modulating the expression of MMP3.
The presence of MT-3 in the zona glomerulosa of pathological adrenal cortex may imply a role in the pathophysiology of aldosterone-producing tissues.
MT-capital I, Ukrainiancapital I, Ukrainiancapital I, Ukrainian increases the amount of active ADAM10 in association with furin, PC7 and PKCalpha.
Upregulation of MT-3 gene expression can inhibit esophageal cancer cell proliferation and induce apoptosis.
The experiments indicate that MT3 is an androgen-upregulated gene, and promotes tumorigenesis of prostate carcinoma cells.
the molecular mechanism for protection against the neuronal cytotoxicity of Abeta(1-42) with copper ions
MT-III expression may have an impact on the pathogenesis of non-small cell lung cancer.
MT-3 modulates the catalytic redox properties of PrP-Cu(II)
Esophageal adenocarcinomas are characterized by frequent epigenetic silencing of MT3.
Metallothionein-III is a specific component of glial cytoplasmic inclusions and is upregulated in multiple system atrophy.
The roles of zinc and metallothionein-3 in autophagy and/or lysosomal function are reviewed.
MT2 diminishes Transthyretin-Abeta binding, whereas MT3 has the opposite effect
the absence of Mt3 reduces Abeta uptake in astrocytes through an abnormality in actin polymerization.
Circadian time and lighting could be involved in the regulation of the expression of melatonin receptors MTNR3 and Rorc.
Mt3 may act through PDE3a to play a key role in Zinc dyshomeostasis and cell death in streptozotocin-treated islets.
Zn released from MT3 may contribute to VEGF induction.
The entire MT3 peptide shows a high capacity to bind Cu(+) , provided that this occurs in a nonoxidative milieux. This reflects a peculiar property of this MT isoform, which senses different Cu contents in the environment in which it is synthesized.
MT-III can help protect against light-induced retinal damage compared to MT-I/II. Some of these effects may be exerted by its antioxidative potency.
MT-3 is able to alter the Tg2576 phenotype in several aspects such as mortality and behavior in a gender-dependent manner.
ZnMt3 in cultured astrocytes may be a normal component of c-Abl activation in EGF receptor signaling
the level of the leptin receptor in the hypothalamus of metallothionein-3-null mice was significantly reduced
Metallothionein-III null mice show attenuation of cadmium-induced severe testicular toxicity, suggesting that lack of MT-III contributes to protection of testis from cadmium.
results indicate that MT3 may play a key role in normal lysosomal function in cultured astrocytes
findings indicate that abnormalities of psychological behavior were observed in the MT-3 knock-out mice
engineered protein has neuroinhibitory activity when introduced into metallothionein-1
a correct MTs homeostasis is pivotal for brain-endocrine-immune response in order to reach successful ageing.
Metallothionein 3 [Mt3]-null mice had increased expression of neurotrophins as well as GAP-43 following cryoinjury. Thus MT-III does not affect the inflammatory response, but it may influence neuronal regeneration during recovery
In contrast to MT-I, MT-III mRNA expression was not significantly altered in any of the models examined suggesting that the various MT isoforms may have different roles in these experimental systems, and perhaps also in human AD.
MT-III isoform, which has a limited tissue distribution, especially in the central nervous system, seems to be implicated in tissue repair and/or protection against critical tissue injury
These findings indicate that neuronal damage was aggravated by reperfusion injury in the MT-III KO mice compared with the wild-type mice, suggesting that MT-III plays anti-oxidative and neuroprotective roles in transient cerebral ischemia.
Expression of MT-1a, MT-2b and MT-3 were significantly higher in high zinc fed pigs.
heavy metal binding protein\; acts as an inhibitor of neurite sprouting and deficiency may play a role in Alzheimer's disease
, growth inhibitory factor
, metallothionein 3 (growth inhibitory factor (neurotrophic))
, metallothionein III
, neurite growth inhibitory factor
, metallothionein 3
, neuronal growth inhibitory factor