Results 131 to 140 of about 628 (165)

3-iodothyronamine (T1AM) is taken up and rapidly metabolized in neuronal cells

open access: yes, 2019
3-iodothyronamine (T1AM) is rapidly catabolized to iodothyroacetic acid after few hours by serum proteins. To avoid a rapid metabolism during any treatment, DMEM devoid of FBS has been used, inducing changes in the cell culture environmental. We evaluated the uptake and the metabolism of different concentrations of T1AM, in presence of supplemented ...
Federica Saponaro   +6 more
openaire   +2 more sources

Effects of 3-iodothyronamine (T1AM) on signaling pathways involved in synaptic plasticity and neuroprotection.

open access: yes, 2017
In mouse, the administration of 3-iodothyronamine (T1AM) had an antiamnestic and prolearning effect. In addition, T1AM rescued long term potentiation (LTP) in enthorinal cortex exposed to the toxic effect of β-amyloid. In the present paper we used a neuronal cell line to evaluate the effect of T1AM on the expression calcium calmodulin dependent kinase ...
Ginevra Sacripanti   +5 more
openaire   +2 more sources

Effects of 3-iodothyronamine (T1AM) on long term potentiation (LTP) postsynaptic signaling cascade

open access: yes, 2018
Aim: In mouse, the administration of 3-iodothyronamine (T1AM) had an antiamnestic and prolearning effect. In addition, T1AM rescued long term potentiation (LTP) in enthorinal cortex exposed to the toxic effect of β-amyloid. In the present study we used a neuronal cell line to evaluate the effects of T1AM on the expression of the calcium calmodulin ...
Ginevra Sacripanti   +6 more
openaire   +2 more sources

The 3-iodothyroacetic acid does not cause change in proteins affected by T1AM.

open access: yes, 2021
The 3-iodothyroacetic acid (TA1) derives from the metabolism of 3-iodothyronamine and it is highly produced in cell culture medium supplemented with fetal bovine serum. Previous results indicated that, in models of brain cell lines, exogenous T1AM can increase the phosphorylation of proteins involved in signaling cascade, but this could be a ...
Bandini L.   +4 more
openaire   +2 more sources

Metabolome dynamics of T1AM, an endogenous thyroid hormone derivative: Effects on lipid metabolism, weight loss, and appetite in mice.

open access: yes, 2012
Objectives: T1AM is an endogenous natural compound that has opposing physiological effects to those of thyroid hormone. T1AM is thought to switch metabolism from carbohydrate to lipid. Due to its recent discovery, detailed actions of T1AM on affected metabolic pathways are still unknown.
Assadi Porter FM   +7 more
openaire   +2 more sources

In the brain of mice, 3-iodothyronamine (T1AM) is converted into 3-iodothyroacetic acid (TA1) and it is included within the signaling network connecting thyroid hormone metabolites with histamine.

open access: yesEuropean Journal of Pharmacology, 2015
3-iodothyronamine (T1AM) and its oxidative product, 3-iodotyhyroacetic acid (TTA1A), are known to stimulate learning and induce hyperalgesia in mice. We investigated whether i)TA1 may be generated in vivo from T1AM, ii) T1AM shares with TA1 the ability ...
Grazia Chiellini   +2 more
exaly   +2 more sources

N-(3-Ethoxy-phenyl)-4-pyrrolidin-1-yl-3-trifluoromethyl-benzamide (EPPTB) prevents 3-iodothyronamine (T1AM)-induced neuroprotection against kainic acid toxicity [PDF]

open access: yesNeurochemistry International, 2019
Thyroid hormone and thyroid hormone metabolites, including 3-iodothyronamine (T1AM) and 3-iodothyroacetic acid (TA1), activate AKT signaling in hippocampal neurons affording protection from excitotoxic damage.
Annunziatina Laurino, Elisa Landucci
exaly   +2 more sources
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3-T1AM signaling in the rat thyrocyte cell line PCCL3

Endocrine Abstracts, 2016
Nancy Schanze   +4 more
openaire   +1 more source

Thyroid hormone metabolite 3-iodothyronamine (T1AM) as an effective repressor of microglia-mediated neuroinflammation

Endocrine Abstracts, 2023
Beatrice Polini   +6 more
openaire   +1 more source

Effects of repeated 3-T1AM treatment on thyrocytes in mice

Experimental and Clinical Endocrinology & Diabetes, 2015
N Schanze   +4 more
openaire   +1 more source

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