C-terminal tensin-like (CTEN) knockin alleviates cystic kidney defects in Tensin-1 knockout mice

Tensins in Kidney Function and Diseases

“…CTEN has been predicted to function as a dominant negative inhibitor of TNS1-3 based on its shorter protein sequence that only shares critical SH2 and PTB domains with other tensins. Surprisingly, our recent mouse studies showed that expression of CTEN in Tns1 -KO mice almost fully rescue all renal phenotypes caused by the lack of TNS1 [ 69 ], indicating that CTEN is in fact a smaller version of tensin and that SH2 and PTB domains carry the essential functions of the tensin family in kidney development/function. Because the SH2 and PTB domains of TNS2 are required for preventing NS development in FVB mice [ 58 ], it will be interesting to test whether CTEN -KI can also rescue Tns2 -KO kidney phenotypes.…”

“…Although CTEN expression eases Tns1 -KO phenotypes, it cannot fully replace TNS1. Compared with CTEN -KI mice, there are still mild defects and a slightly shorter lifespan in Tns1 -KO/ CTEN -KI mice [ 69 ]. Both TNS1 and CTEN contain a focal adhesion targeting site in their N-terminal regions, albeit no sequence similarity between them.…”