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Gliadin p31-43 TFA

CAS No. :

MCE 站：Gliadin p31-43 TFA

产品活性：Gliadin p31-43 TFA 是一种未消化的麦醇溶蛋白肽，可诱导肠道内的先天性免疫反应并干扰内吞运输。Gliadin p31-43 TFA 可用于乳糜泻的研究。

研究领域：Others

作用靶点：Others

In Vitro: Gliadin p31-43 (100 μg/mL; 30 minutes-6 hours) treatment induces the MyD88/TLR7 complexes, ａnd activates downstream signalling by activating MAPKs, ERK, JNK ａnd p38). Gliadin p31-43 increases the levels of the phosphorylated forms of pY-ERK, JNK (pY-JNK) ａnd p38 (pY-p38).
Gliadin p31-43 treatment increases NF-κB phosphorylation in CaCo-2 cells from 0.45 in control cells to 0.86. Gliadin p31-43 treatment induces a significant increase in levels of the MxA protein. The levels of the IFN-α 7 ａnd 17 mRNAs are also analysed after Gliadin p31-43 treatment.
In CaCo-2 cells, Gliadin p31-43 localizes to the early endosomes ａnd delays vesicular trafficking. Gliadin p31-43 interferes with the correct localization of the growth factor regulated tyrosine kinase substrate (HRS) to early endosomes, delaying the maturation of the endocytic vesicles.

In Vivo: Gliadin p31-43 (10 μg; intraluminally injection) shows a sequence-specific spontaneous ability to form structured oligomers ａnd aggregates in vitro ａnd induced activation of the apoptosis-associated speck-like (ASC) complex.
The increment of IL-1β indicates the activation of the inflammasome caspase-1 pathway in the small intestine mucosa by oral administration of Gliadin p31-43 (20 μg) in wild type C57Bl/6 mice. Gliadin p31-43 has an intrinsic propensity to form oligomers which trigger the NLRP3 inflammasome.

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