High impact information on Ctnna2

• The deletion includes part of Catna2, encoding alpha N-catenin, a protein that links the classical cadherins to the neuronal cytoskeleton [1].
• Expression of a Catna2 transgene in cdf/cdf mice restored normal cerebellar and hippocampal morphology, prepulse inhibition and fear conditioning [1].
• Here we show that alpha N-catenin, a linker between cadherin adhesion receptors and the actin cytoskeleton, is essential for stabilizing dendritic spines in rodent hippocampal neurons in culture [2].
• Stability of dendritic spines and synaptic contacts is controlled by alpha N-catenin [2].
• Conversely, alpha N-catenin overexpression in dendrites reduced spine turnover, causing an increase in spine and synapse density [2].

Biological context of Ctnna2

• We also localized the mouse alpha N-catenin gene to chromosome 6 [3].
• During embryogenesis, alpha N-catenin was first detected in nerve fibers of cranial and dorsal root ganglia and also in early neurons in the neural tube, including motor neurons [3].
• We isolated cDNAs encoding mouse homologues of chicken alpha N-catenin, a protein associated with the cadherin cell adhesion molecules, and identified two isoforms of this protein [3].
• Here we report the effects of alpha N-catenin gene deficiency on brain morphogenesis [4].

Anatomical context of Ctnna2

• Furthermore, alpha N-catenin, a cadherin-associated protein, was found to occur at the roof plate of the mesencephalon and diencephalon, coinciding with Wnt-1 expression [5].
• Alteration of E-cadherin and alpha N-catenin immunoreactivity in the mouse spinal cord following peripheral axotomy [6].
• In the absence of alpha N-catenin, spine heads were abnormally motile, actively protruding filopodia from their synaptic contact sites [2].
• For example, the ependymal layers of the neural tube generally expressed low levels of alpha N-catenin except at the inner limiting membrane facing the central canal, whereas the floor and roof plate exhibited strong expression of this protein at various portions of the central nervous system [3].
• The choroid plexus was devoid of alpha N-catenin [3].

Associations of Ctnna2 with chemical compounds

• Administration of nerve growth factor (NGF) rescued the immunoreactivity of substance P, which is known to disappear after peripheral axotomy, but not influence that of both E-cadherin or alpha N-catenin [6].
• Tetrodotoxin (TTX), a neural activity blocker, suppressed the synaptic accumulation of alpha N-catenin, whereas bicuculline, a GABA antagonist, promoted it [2].
• E-Cadherin and alpha-N-catenin, synapse-related molecules, were intensely expressed in the spinal dorsal horn of the DCP-treated side [7].

Other interactions of Ctnna2

• Wnt-1-dependent regulation of local E-cadherin and alpha N-catenin expression in the embryonic mouse brain [5].
• On the contrary, alpha N-catenin expression in the dorsal midline was suppressed in these mutants [5].
• In the alpha N-catenin-negative regions, another subtype of alpha-catenin, alpha E-catenin, was expressed [3].

Analytical, diagnostic and therapeutic context of Ctnna2

• The expression of alpha N-catenin in the superficial dorsal horn was similarly reduced by day 7 after axotomy, but recovered by day 63 after nerve ligature [6].
• Immunostaining and in situ hybridization analyses revealed that the mouse alpha N-catenin was expressed almost exclusively in the nervous system [3].

References