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Nickel reduces calcium dependent dimerization in neural cadherin
M P Dukes1, R K Rowe, T Harvey
1Department of Chemistry and Biochemistry, University of Mississippi, University, MS 38677, USA. spedigo@olemiss.edu.
Metallomics : Integrated Biometal Science
|January 10, 2019
Summary
Divalent cations like magnesium and nickel affect neural cadherin (N-cadherin) function. Nickel significantly reduces N-cadherin
Area of Science:
- Cell Biology
- Biochemistry
- Neuroscience
Background:
- Cadherins are essential transmembrane proteins mediating cell-cell adhesion in adherens junctions.
- Calcium ions are critical for cadherin binding and the linkage of actin cytoskeletons in tissues.
- The extracellular microenvironment's complexity suggests other divalent cations may influence cadherin function.
Purpose of the Study:
- To investigate the impact of magnesium (Mg2+) and nickel (Ni2+) on calcium-dependent neural cadherin (N-cadherin) dimerization.
- To characterize how physiological and neurotoxic divalent cations affect N-cadherin's calcium-binding affinity.
Main Methods:
- Studied the effects of Mg2+ and Ni2+ on N-cadherin function in vitro.
- Performed competitive binding assays to determine dissociation constants (Kd) for Ni2+ and Mg2+.
- Quantified the influence of these cations on calcium-induced N-cadherin dimerization.
Main Results:
- Physiological magnesium levels showed minimal impact on N-cadherin's calcium-binding affinity and dimerization.
- Nickel ions, even at lower concentrations, significantly decreased N-cadherin's apparent calcium-binding affinity and dimerization.
- Apparent dissociation constants were 0.2 mM for nickel and 2.5 mM for magnesium, reflecting extracellular concentrations.
Conclusions:
- Extracellular divalent cations, including physiological magnesium and non-physiological nickel, can attenuate calcium-induced N-cadherin dimerization.
- Nickel's potent effect highlights potential disruption of cell-cell adhesion in neurological synapses and other tissues.
- Understanding these interactions is crucial for comprehending cell adhesion dynamics in diverse physiological and pathological contexts.
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