- PA5-42383 - Invitrogen Antibodies PEMT antibody

Kim YC, Seok S, Byun S, Kong B, Zhang Y, Guo G, Xie W, Ma J, Kemper B, Kemper JK
Nature communications 2018 Feb 7;9(1):540

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of rat liver cell lysate using an anti-PEMT polyclonal antibody (Product # PA5-42383). Primary Antibody Dilution: 1:2000; Secondary Antibody: Anti-rabbit HRP; Secondary Antibody Dilution: 1:15000.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of rat liver cell lysate using an anti-PEMT polyclonal antibody (Product # PA5-42383). Primary Antibody Dilution: 1:1000; Secondary Antibody: Anti-rabbit HRP; Secondary Antibody Dilution: 1:15000.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of human 721_B cell lysate using an anti-PEMT polyclonal antibody (Product # PA5-42383).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 8 Elevated AHR, PEMT, and PC levels in livers of NAFLD steatosis and NASH patients. a mRNA levels of PEMT , GNMT , and AHR in liver samples of 15 normal, 15 simple steatosis, and 15 severe NASH-fibrosis patients were determined by qRT-PCR. b Protein levels of PEMT, AHR, phosphorylated T55-SHP, and SHP in liver extracts from 5 samples each randomly pooled from 3 individuals (total 15 individuals) were analyzed by IB analysis (top) and the band intensities were quantified (bottom). The same normal samples were analyzed as controls in the two separate gels. Full size immunoblots are in Supplementary Figure 12e . c Hepatic PC and PE levels were determined by LC-MS and the ratios of PC/PE calculated. Means +- SD are shown ( n = 15), and statistical significance was measured using the b (bottom) Student's t -test or a , c one-way ANOVA with the FDR post-test. * P < 0.05, ** P < 0.01, NS, not statistically significant. d Model: Temporal transcriptional regulation of the 1C cycle genes by a postprandial AhR-SHP axis. Nuclear levels of AhR are increased early after feeding by insulin/PKB signaling and nuclear AhR mediates transcriptional induction of 1C cycle genes, including Pemt and AhR , which results in increased hepatic PC and decreased SAM levels. In the late fed state, SHP blocks this AhR action through FGF15/19 signal-induced phosphorylation at T55

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 7 Downregulation of Pemt or overexpression of SHP blunts AhR-mediated increases in PC levels and liver steatosis in mice fed HF/HF. a Experimental outline: Mice ( n = 5 mice per group) were fed a HF/HF diet for 8 weeks and infected with the indicated adenovirus. For the Ad-CA-AhR injection, Ad-GFP was added so that the same number of viral particles were injected for each group. At 3 weeks after adenoviral injection, livers were collected for further analyses. b Samples from three mice per each group were randomly selected and analyzed by IB (left) and quantification of the bands is shown (right). Full size immunoblots are in Supplementary Figure 12d . c Representative images of livers from the experimental groups. d Oil Red-O staining of frozen liver sections. Scale bar: 100 uM. e Liver TG levels. f mRNA levels of Pemt, Gnmt, and Cyp1a1 as determined by qRT-PCR. g Ratios of SAH/SAM and PC/PE as calculated from levels of these metabolites determined by LC-MS ( n = 5). Means +- SD are shown ( n = 5 mice), and statistical significance was measured using the b - (right), e - g one-way ANOVA with the FDR post-test. * P < 0.05, ** P < 0.01, NS, not statistically significant

PA5-42383