Recombinant Human ICAM5 protein

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

ICAM5 also known as Telencephalin is an intercellular adhesion molecule with a molecular mass of approximately 130 kDa. This protein is mainly expressed in the brain specifically in neurons of the telencephalon region. ICAM5 belongs to the immunoglobulin superfamily and plays a role in cell-cell adhesion. It does not demonstrate tight adherence like other ICAMs which suggests its specific function might differ from other ICAM family members.

Biological function summary

ICAM5 participates in neuron-neuron adhesion processes. It plays a significant role in the development and maintenance of synaptic structures in the nervous system. ICAM5 does not form a complex with other proteins in its functioning. It contributes to the organization and stabilization of dendritic spines which are important for synaptic plasticity and neural communication. This involvement highlights the importance of ICAM5 in neural development and synaptic function.

Pathways

ICAM5 integrates into signaling pathways related to neuronal development and synaptic plasticity. It is a part of the adhesion and cell recognition processes in neural systems. Through its involvement ICAM5 associates with pathways like the glutamatergic synapse pathway. Additionally ICAM5 shows a connection with proteins involved in membrane transport and neuronal signaling such as NMDARs (N-methyl-D-aspartate receptors) emphasizing its role in synaptic modulation.

ICAM5 relates to conditions affecting the nervous system such as schizophrenia and Alzheimer's disease. Studies indicate alterations in ICAM5 expression levels in patients with these diseases suggesting a potential impact on synaptic integrity and function. In Alzheimer's disease ICAM5 interacts with pathways involving beta-amyloid peptide accumulation indicating a possible connection with oxidative stress and neurodegenerative processes. In schizophrenia disruptions in ICAM5 associations with neural adhesion molecules could affect synaptic signaling and stability contributing to cognitive deficits.