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these results demonstrate that MT2 plays a role in CD4+ T cell activation by transducing reactive oxygen species signals into an increased [Zn2+]i that subsequently affects downstream effector function
blockade of metallothioneins 1 and 2 constitutes a promising approach for the treatment of conditions which result in muscle atrophy.
Cardioprotective effects of MT1/2 seem to be exerted via modulation of contractile elements, antioxidative enzymes, inflammatory response, and myocardial remodeling.
Metallothioneins may have a protective role against post-burn inflammation and inflammatory organ damage, at least partly through inhibiting the p38 MAPK signaling.
Enhanced senescence due to absence of metallothionein genes may shorten lifespan.
The MT2 receptor activates Akt/GSK-3beta/CRMP-2 signaling and is necessary and sufficient to mediate functional axonogenesis and synaptic formation in central neurons.
MT1/2 deficiency aggravated depleted uruanium-induced nephrotoxicity, and the molecular mechanisms appeared to be related to the increased oxidative stress and apoptosis, and decreased SGLT expression.
Zinc-binding MT1 and MT2 are key modulators of Fc epsilonRI-induced basophil production of IL-4.
Metallothionein blocks oxidative DNA damage induced by acute inorganic arsenic exposure
the metal binding abilities of mouse MT2 (mMT2) with divalent (Zn(II) and Cd(II)) and monovalent (Cu(I)) ions were analyzed and compared to those of the mouse MT1 (mMT1) isoform.
The results of this study suggest that metallothioneins may play a key role in protecting the kidney against high glucose-induced ROS and subsequent inflammation in diabetic nephropathy.
these results demonstrate that MT-I/II knockout mice are more vulnerable to cadmium-induced fetal growth retardation.
These data indicate that metallothioneins play an important role in the prevention of colonic mucosal inflammation in a mouse model of dextran sulfate sodium-induced colitis.
Metallothioneins act as negative regulators for IL-27-induced Tr1 cells.
Zn deficiency in utero induces fetal epigenetic alterations of Mt2 gene and these changes are being stored as an epigenetic memory until adulthood.
MT1 + 2 effectively alters the amyloid cascade, survival, body weight, and behavior in a complex manner
Down-regulation of MT1 and MT2 after electromagnetic fields in mouse testis might be followed by some consequences that result in infertility.
MT-I/II is up-regulated in the liver after brain injury and modulates the amount of zinc that is sequestered to the liver.
the absence of MT1 and MT2 has no unfavorable effect on ischemic brain injury
Data suggest that metallothionein (MT)-I/II(-/-) mice have altered immune function and provide a new hypothesis that this alteration is partly responsible for the differences observed in MT-I/II(-/-) mice after brain injury relative to wild type mice.
Report expression of similar to metallothionein-B(smt-B) upon cadmium exposure and cold shock in zebrafish (Danio rerio).
mt2 and smtb may play an important role in neurogenesis and neuroprotection.
data not only reveal a non-canonical function of Mt2 in angiogenesis, but also propose Mt2 as a novel regulator of vegfc expression.
Metallothioneins have a high content of cysteine residues that bind various heavy metals\; these proteins are transcriptionally regulated by both heavy metals and glucocorticoids.
, Metallothionein 2
, metallothionein IIA
, metallothionein IIB
, metallothionein II