Authors working quickly on the TRB3, a center gene for rapid understanding!

Homocystein can block cell proliferation by upregulating p27 which reportedly increases phosphorylation of AKT.Phosphorylation of the AKT also happens with upregulation by Homocystein of TRB3, however the consequential effect of TRB3 upregulation leads to Endoplasmic Reticulum stress (Zou et al).  It is unclear that when TRB3 is busy intervening in the cell proliferation blockage, it also effectively causes the stress mentioned above.   We know that homocystein induced hypercoagulation, ?does reticulum induces stress at the center of Atheroma deposit in blood vessel?  putting TRIB3 blockage at the center of events?'Homocysteine-induced TRB3 expression was mediated by the cAMP/cAMP response element-binding protein (CREB) pathway." per Zou.
giving 3 ways to affect
1.suppression of TRIB directly by gene interference
or by troubling the CREB as noted by Zou et al.
2.blocking phosphorylation of the AKT
3.blocking p27
4.Zhang et al "However, expression of p-AKT protein increased when TRB3 was inhibited by TRB3 shRNA inhibition."  proving blocking RNA could prove effective in preventing Atheroma and cell proliferation through homocystein effect

This TRB3 does not stop there!
Cravero et al:"TRB3, a tribbles homolog, has been shown to inhibit IGF-1-mediated activation of Akt in HEK 293 cells. This study was undertaken to determine if TRB3 is expressed in chondrocytes, and whether the chondrocyte response to IGF-1 is reduced by TRB3."
By targeting or acting with the "terrible" IGF1, TRB3 is in the nix of pathologies
its interactions with the NOTCH and CSNK2B are under close review....
how this TRB3 associate with TIAF1 and RELA
well will see as this story unfolds

What is the TRB3 behavior in the Cordon? and how this may affect the stem cells?