bioRxiv Science⌕ Search

Biology subjects

Jambrovics, K.

Publications and source records attributed to Jambrovics, K..

2 recordsLinked to original sources

The transglutaminase 2 interactome in HUVECs suggests its participation in an RNA-binding protein network

Human transglutaminase 2 (TG2) is a multifunctional protein that exhibits various protein-modifying catalytic and protein-protein interaction properties. HUVECs express high levels of TG2, and identification of its interacting partners may provide mechanistic insight into its role in endothelial functions such as adhesion, migration, angiogenesis, and NO homeostasis. For this purpose, two approaches were employed. Firstly, bacterially expressed, site-specifically biotinylated recombinant TG2 was mixed with HUVEC extract to isolate interacting partners by affinity chromatography. Secondly, endogenous TG2 was silenced, and to ensure high antibody affinity, a triple Flag-tagged transgenic TG2-expressing HUVEC line was created, allowing stable binding to anti-Flag antibody-coated agarose for isolating TG2-associated protein complexes. Altogether, 170 and 356 TG2-associated proteins were identified, respectively, with 86 proteins overlapping between the two approaches. The most enriched GO Molecular Functions of cellularly assembled TG2-interacting proteins confirm TG2s involvement in cell-cell and cell-extracellular matrix communication, adhesion, cytoskeleton organisation, and exosome secretion. Stabilising the catalytically inactive closed TG2 conformation reduced the number of TG2 interactors, whereas stabilising its open form increased the number of associated membrane transporters. Significant enrichment of RNA-binding proteins associated with TG2 was observed in all experiments, and a 42% overlap between the TG2 interactome and previously identified RNA-binding proteins in HUVEC was noted. Considering the recently recognised RNA-binding ability of TG2, our results suggest that TG2 participates in post-transcriptional regulations as a central hub within the network of RNA-binding proteins. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/672361v1_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@169329corg.highwire.dtl.DTLVardef@179d5d4org.highwire.dtl.DTLVardef@1c58f9aorg.highwire.dtl.DTLVardef@156def0_HPS_FORMAT_FIGEXP M_FIG Cellularly assembled TG2-associated proteins were isolated and identified from endogenous TG2-silenced (eTG2-KD) and transgenic, high-affinity antibody, triple Flag-tagged TG2 (3F-TG2) expressing HUVECs under untreated conditions and after NC9 or GTP{gamma}S inhibitor treatments, which stabilise its open or closed conformation, respectively. TG2 interactome analysis suggests that it acts as a central hub in an RNA-binding protein (RBP) network. C_FIG

molecular biology↗

Transglutaminase 2 associated with PI3K and PTEN in a putative membrane-bound signalosome platform blunts cell death

Atypically expressed transglutaminase 2 (TG2) has been identified as a poor prognostic factor in a variety of cancers. In this study, we evaluated the contribution of TG2 to the prolonged cell survival of differentiated acute promyelocytic leukaemia (APL) cells in response to the standard treatment with combined retinoic acid (ATRA) and arsenic trioxide (ATO). We report that one advantage of ATRA + ATO treatment compared to ATRA alone diminishes the amount of activated and non-activated CD11b/CD18 and CD11c/CD18 cell surface integrin receptors. These changes suppress ATRA-induced TG2 docking on the cytosolic part of CD18 {beta}2-integrin subunits and reduce cell survival. In addition, TG2 overexpresses and hyperactivates the phosphatidylinositol-3-kinase (PI3K), phospho-AKT S473, and phospho-mTOR S2481 signalling axis. mTORC2 acts as a functional switch between cell survival and death by promoting the full activation of AKT. We show that TG2 presumably triggers the formation of a signalosome platform, hyperactivates downstream mTORC2-AKT signalling, which in turn phosphorylates and inhibits the activity of FOXO3, a key pro-apoptotic transcription factor. In contrast, the absence of TG2 restores basic phospho-mTOR S2481, phospho-AKT S473, PI3K, and PTEN expression and activity, thereby sensitising APL cells to ATO-induced cell death. We conclude, that atypically expressed TG2 may serve as a hub, facilitating signal transduction via signalosome formation by the CD18 subunit with both PI3K hyperactivation and PTEN inactivation through the PI3K PTEN cycle in ATRA-treated APL cells.

cancer biology↗