Fig 1: TRIM18 interacts with protein tyrosine phosphatases (PTP1B) and promotes PTP1B ubiquitination. (A) HK-2 cells were treated with HG and transduced with indicated vectors, and then TRIM18, SHP-1, SOCS1, PTP1B, and PIAS1 expression was measured. (B,C) Cell lysates were immunoprecipitated and then blotted with the indicated antibodies. (D–F) Cells were transduced with indicated vectors with/without 10 µM MG132, and then PTP1B expression was measured. (G) PTP1B was immunoprecipitated and immunoblotted. Values are presented as mean ± SD. n = 3/group. ***p < 0.001 vs. shNC or vector+vehicle. ###p < 0.001 vs. oeTRIM18+vehicle.
Fig 2: TRIM18-regulated STAT3 signaling pathway via PTP1B promotes renal EMT, inflammation, and fibrosis. HK-2 cells were transduced with the indicated vectors, and the (A) cell morphology, (B–D) levels of Hyp, IL-6, and TNF-a, and (E,F) expression of p-STAT3, PTP1B, CTGF, and a-SMA were measured. Scale bar: 100 µm. (G) Schematic representation of the regulation of inflammation and fibrosis of HG-induced HK-2 cells via the TRIM18/PTP1B/STAT3 pathway. Values are presented as mean ± SD. n = 3/group. ***p < 0.001 vs. vector. ###p < 0.001 vs. oeTRIM18.
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