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Autophagy-related proteins(Atg) are involved in regulation of dsDNA-induced innate immune responses. Atg9a regulates membrane trafficking involved in the movement of STING and dsDNA-induced production of type I IFNs. Autophagosomes target and engulf bacteria-containing vacuoles in a STING-dependent manner and mediate autolysosomal degradation of invading bacteria.
Autophagosomes also target and engulf ubiquitinated ASC and mediate autolysosomal degradation of the AIM2-inflammasome to suppress dsDNA-induced production of inflammatory cytokines. However, it is important to note that these studies mainly utilized an in vitro approach. Thus, the contribution of autophagy-related proteins to the regulation of dsDNA-induced innate immune responses in vivo remains unclear. Further studies using conditional knockout mice are required to clarify the role of autophagy-related proteins in the regulation of dsDNA-induced innate immune responses.
Cat. No. | Product Name | CAS No. | Information |
---|---|---|---|
GY03994 |
Cambendazol |
26097-80-3 | NSC 377071 (NSC-377071, NSC377071, Cambendazole) is a novel ATG4B antagonist that inhibits autophagy, with no effect on mTOR and PI3K activities; directly inhibits cellular ATG4B activity induced by starvation or rapamycin and suppresses the lipidation of LC3B and autophagosome formation in response to starvation, suppresses Saos-2 osteosarcoma growth in vivo. |
GY02950 |
FMK-9a |
1955550-51-2 | FMK-9a (FMK9a) is a potent, selective, covalent peptidomimetic inhibitor of ATG4B (Autophagin-1) with IC50 of 80 nM in TR-FRET assay; displays no activity against the aspartic protease, serine proteases, metalloproteases and the 20S proteasome, inhibits cathepsin B and calpain with submicromolar IC50 (0.1-0.2 uM); covalently binds to Cys74 and inactivates ATG4B proteolytic activity, has an IC50 of 15 nM in the cellular LRA assay. |
GY06429 |
S130 |
1160852-22-1 | S130 (ATG4B inhibitor S130) is a potent, specific ATG4B inhibitor with IC50 of 3.24 uM, shows strong affinity (Kd=4 uM) and specifically suppresses the activity of ATG4B, but not other proteases; displays no inhibitory effects on cysteine proteases such as CASP3 (caspase 3), CASP8 (caspase 8) and CASP9 (caspase 9), or aspartic proteases; does not cause the impairment of autophagosome fusion, nor does it result in the dysfunction of lysosomes; causes cell death of colorectal cancer cells in vitro and in vivo. |
GY06369 |
NSC 185058 |
39122-38-8 | NSC 185058 (NSC185058, NSC-185058, 2-Pyridinecarbothioamide) is a novel ATG4B antagonist that inhibits autophagy with IC50 of 50 uM, with no effect on mTOR and PI3K activities; directly inhibits cellular ATG4B activity induced by starvation or rapamycin and suppresses the lipidation of LC3B and autophagosome formation in response to starvation, suppresses Saos-2 osteosarcoma growth in vivo; markedly slows tumor growth and provides a significant survival benefit in GBM xenografts combined with radiotherapy. |
GY05597 |
LV-320 |
LV-320 (LV320) is a novel potent, cell-active, allosteric inhibitor of the autophagy-related cysteine protease ATG4B with IC50 of 24.5 uM in ATG4B cleavage assays; LV-320 binds to ATG4B and is an uncompetitive inhibitor of ATG4B with Kd of 16 uM; blocks starvation-induced autophagic fux in vitro; also inhibit ATG4A with an IC50 of 35.5 uM, but does not shows meaningful inhibition for caspase-3 or cathepsin B; LV-320 reduces autophagic fux in vitro and is bioavailable and active in vivo, LV-320 is a relevant chemical tool to study the various roles of ATG4B in cancer and other contexts. |
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