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Phospho-TAK1 (Ser412) Antibody

RRID:AB_2140096

Antibody ID

AB_2140096

Target Antigen

MAP3K7 human, rat, mouse

Proper Citation

(Cell Signaling Technology Cat# 9339, RRID:AB_2140096)

Clonality

polyclonal antibody

Comments

Applications: W, IP. Consolidation on 9/2016: AB_2250296.

Host Organism

rabbit

Vendor

Cell Signaling Technology

Cat Num

9339 also 9339S, 9339L

Publications that use this research resource

Th9 Cells Represent a Unique Subset of CD4+ T Cells Endowed with the Ability to Eradicate Advanced Tumors.

  • Lu Y
  • Cancer Cell
  • 2018 Jun 11

Literature context:


Abstract:

The antitumor effector T helper 1 (Th1) and Th17 cells represent two T cell paradigms: short-lived cytolytic Th1 cells and "stem cell-like" memory Th17 cells. We report that Th9 cells represent a third paradigm-they are less-exhausted, fully cytolytic, and hyperproliferative. Only tumor-specific Th9 cells completely eradicated advanced tumors, maintained a mature effector cell signature with cytolytic activity as strong as Th1 cells, and persisted as long as Th17 cells in vivo. Th9 cells displayed a unique Pu.1-Traf6-NF-κB activation-driven hyperproliferative feature, suggesting a persistence mechanism rather than an antiapoptotic strategy. Th9 antitumor efficacy depended on interleukin-9 and upregulated expression of Eomes and Traf6. Thus, tumor-specific Th9 cells are a more effective CD4+ T cell subset for adoptive cancer therapy.

Funding information:
  • NCI NIH HHS - K99 CA190910()
  • NCI NIH HHS - R00 CA190910()
  • NHGRI NIH HHS - R01 HG003523-03(United States)

Diets Containing α-Linolenic (ω3) or Oleic (ω9) Fatty Acids Rescues Obese Mice From Insulin Resistance.

  • Oliveira V
  • Endocrinology
  • 2015 Nov 17

Literature context:


Abstract:

Subclinical systemic inflammation is a hallmark of obesity and insulin resistance. The results obtained from a number of experimental studies suggest that targeting different components of the inflammatory machinery may result in the improvement of the metabolic phenotype. Unsaturated fatty acids exert antiinflammatory activity through several distinct mechanisms. Here, we tested the capacity of ω3 and ω9 fatty acids, directly from their food matrix, to exert antiinflammatory activity through the G protein-coupled receptor (GPR)120 and GPR40 pathways. GPR120 was activated in liver, skeletal muscle, and adipose tissues, reverting inflammation and insulin resistance in obese mice. Part of this action was also mediated by GPR40 on muscle, as a novel mechanism described. Pair-feeding and immunoneutralization experiments reinforced the pivotal role of GPR120 as a mediator in the response to the nutrients. The improvement in insulin sensitivity in the high-fat substituted diets was associated with a marked reduction in tissue inflammation, decreased macrophage infiltration, and increased IL-10 levels. Furthermore, improved glucose homeostasis was accompanied by the reduced expression of hepatic gluconeogenic enzymes and reduced body mass. Thus, our data indicate that GPR120 and GPR40 play a critical role as mediators of the beneficial effects of dietary unsaturated fatty acids in the context of obesity-induced insulin resistance.

Funding information:
  • NIDDK NIH HHS - P30 DK020572(United States)
  • NIDDK NIH HHS - P30 DK090971(United States)