The first Zn finger coordinates a Zn2+ ion in a unique conformation.

A new water-insoluble bi-metallic coordination polymer was simply prepared via polymerization-precipitation of molybdenum complex building blocks with Zn2+ cation.

In this work, we present genetically encoded sensors for Zn2+ based on the principle of fluorescence resonance energy transfer.

However, two distinct Zn2+ binding sites, one competitive and one noncompetitive, could also give rise to the dual antagonism.

Our results suggest that mitochondria serve as a source of and a sink for Zn2+ signals under different cellular conditions.

The apparent mixed antagonism may arise from different Ki values for the binding of Zn2+ to non-agonist-bound or agonist-bound receptors.

Synergistic combinations of Zn2+ and the tetraphosphonate are found to form films that protect against the corrosion of carbon steels.

The transition metal Zn2+ is differentially distributed in the central nervous system, where it is proposed to be a neuromodulator.

In the following step, the newly generated Zn2 bound hydroxide makes the reverse attack, resulting in the regeneration of the bridging hydroxide.

However, there has been relatively little research investigating the effects of Aβ self-assembly and toxicity inhibitors in the presence of Zn2+.

Purified rRbPGRP2 interactions with bacteria and inhibited the growth of bacteria in the presence of Zn2+.

The prevention of apoptosis by Zn2+ has generally been attributed to its inhibition of an endonuclease acting in the late phase of apoptosis.

Zinc finger proteins, comprising one of the largest transcription factor families, are known for their finger-like structure and their ability to bind Zn2+.

Micromolar concentrations of extracellular Zn2+ are known to antagonize native NMDA receptors via a dual mechanism involving both a voltage-independent and a voltage-dependent inhibition.

Here, we asked whether three CTFs shown to be potent inhibitors of Aβ42 toxicity maintained their activity in the presence of Zn2+.

In this study, we have identified in Zn2+ finger transcription factor RU49 as a definitive marker for the cerebellar granule neuron lineage.