TCDB is operated by the Saier Lab Bioinformatics Group

Shisa6 of 500 aas and 2 TMSs, one N-terminal and one at position 176 - 195.  Interacts with AMPA receptors (TC# 1.A.10) at post synaptic sites and prevents desensitization (Klaassen et al. 2016).

Shisa6 of Homo sapiens

Shisa8 protein of 492 aas and 2 TMSs with a Class II PDZ domain. Regulates short term neuronal synaptic plasticity.  Present in the olfactory bulb and cerebellum.  Involved in prolongation of deactivation and an increase in desensitization of GluA2 without change in that of GluA1. It slowed recovery from desensitization, enhanced of glutamate potency, and reducted cyclothiazide potency (Kato and Witkin 2018).

Shisa8 of Homo sapiens

Shisa9, or CKAMP44 of 424 aas and 2 TMSs. Regulator of short-term neuronal synaptic plasticity in the dentate gyrus. It associates with AMPA receptors (ionotropic glutamate receptors; TC#1/A/10) in synaptic spines and promotes AMPA receptor desensitization at excitatory synapses. It is found in the dentate gyrus and olfactory bulb. It has a class II PDZ domain and is expressed in a majority of regions of the brain.  It slows recovery from desensitization, enhances glutamate potency and reduces cyclothiazide potency and efficacy (Kato and Witkin 2018).

Shisa9 of Homo sapiens

Shisa7 of 538 aas and 2 TMSs.  It is a AMPAR modulatory protein affecting channel kinetics of AMPARs, necessary for synaptic hippocampal plasticity and memory recall (Schmitz et al. 2017). Shisa7 controls receptor abundance at synapses and speeds up the channel deactivation kinetics. Shisa7 also potently enhances the action of diazepam, a classic benzodiazepine, on GABAARs. Genetic deletion of Shisa7 selectively impairs GABAergic transmission and diminishes the effects of diazepam in mice. Thus, Shisa7 regulates GABAAR trafficking, function, and pharmacology (Han et al. 2019). A kinetic basis for how Shisa7 modifies temporal attributes of GABAergic transmission at the single-channel level has been described (Castellano et al. 2022).

Shisa7 of Homo sapiens

Shesa-1 (Shisa1) of 269 aas and 1 TMS. It is required for head formation during gastrulation. It functions as an inhibitor for the caudalizing signals wnt and fgf, but does not inhibit bmp, activin and nodal signaling in the head formating process. It induces retention of fzd8 in the endoplasmic reticulum and inhibits trafficking of fzd8 to the cell surface (Yamamoto et al. 2005).

Shisa1 of Xenopus laevis (African clawed frog)

Shisa-2 (Shisa2) of 288 aas and 2 TMSs, an N-terminal targetting signal, and a central TMS, common to other Shisa proteins.  It plays an essential role in the maturation of presomitic mesoderm cells by individual attenuation of both Fgf and Wnt signaling. It inhibits both Wnt and Fgf signaling through the regulation of protein maturation and cell surface transport of their receptors within the endoplasmic reticulum (Nagano et al. 2006).

Shisa2 of Xenopus laevis (African clawed frog)