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c-Myc Antibody


Antibody ID


Target Antigen

Nol3 human, rat, mouse

Proper Citation

(Cell Signaling Technology Cat# 9402, RRID:AB_2151827)


polyclonal antibody


Applications: W, IP, ChIP. Consolidation on 10/2018: AB_10693752, AB_2151827.

Host Organism



Cell Signaling Technology

Sam68 Allows Selective Targeting of Human Cancer Stem Cells.

  • Benoit YD
  • Cell Chem Biol
  • 2017 Jul 20

Literature context:


Targeting of human cancer stem cells (CSCs) requires the identification of vulnerabilities unique to CSCs versus healthy resident stem cells (SCs). Unfortunately, dysregulated pathways that support transformed CSCs, such as Wnt/β-catenin signaling, are also critical regulators of healthy SCs. Using the ICG-001 and CWP family of small molecules, we reveal Sam68 as a previously unappreciated modulator of Wnt/β-catenin signaling within CSCs. Disruption of CBP-β-catenin interaction via ICG-001/CWP induces the formation of a Sam68-CBP complex in CSCs that alters Wnt signaling toward apoptosis and differentiation induction. Our study identifies Sam68 as a regulator of human CSC vulnerability.

Foxp3 Reprograms T Cell Metabolism to Function in Low-Glucose, High-Lactate Environments.

  • Angelin A
  • Cell Metab.
  • 2017 Jun 6

Literature context:


Immune cells function in diverse metabolic environments. Tissues with low glucose and high lactate concentrations, such as the intestinal tract or ischemic tissues, frequently require immune responses to be more pro-tolerant, avoiding unwanted reactions against self-antigens or commensal bacteria. T-regulatory cells (Tregs) maintain peripheral tolerance, but how Tregs function in low-glucose, lactate-rich environments is unknown. We report that the Treg transcription factor Foxp3 reprograms T cell metabolism by suppressing Myc and glycolysis, enhancing oxidative phosphorylation, and increasing nicotinamide adenine dinucleotide oxidation. These adaptations allow Tregs a metabolic advantage in low-glucose, lactate-rich environments; they resist lactate-mediated suppression of T cell function and proliferation. This metabolic phenotype may explain how Tregs promote peripheral immune tolerance during tissue injury but also how cancer cells evade immune destruction in the tumor microenvironment. Understanding Treg metabolism may therefore lead to novel approaches for selective immune modulation in cancer and autoimmune diseases.

Funding information:
  • NCI NIH HHS - R33 CA182384()
  • NIAID NIH HHS - K08 AI095353()
  • NIAID NIH HHS - P01 AI073489()
  • NIAID NIH HHS - R01 AI073938()
  • NIAID NIH HHS - R56 AI095276()
  • NIDDK NIH HHS - K08 DK092282()
  • NIDDK NIH HHS - K23 DK101600()
  • NIDDK NIH HHS - R01 DK098656()
  • NIDDK NIH HHS - R01 DK106243()
  • NIH HHS - R01 OD010944()
  • NIMH NIH HHS - R01 MH108592()
  • NINDS NIH HHS - R01 NS021328()

De-repression of the RAC activator ELMO1 in cancer stem cells drives progression of TGFβ-deficient squamous cell carcinoma from transition zones.

  • McCauley HA
  • Elife
  • 2017 Feb 21

Literature context:


Squamous cell carcinomas occurring at transition zones are highly malignant tumors with poor prognosis. The identity of the cell population and the signaling pathways involved in the progression of transition zone squamous cell carcinoma are poorly understood, hence representing limited options for targeted therapies. Here, we identify a highly tumorigenic cancer stem cell population in a mouse model of transitional epithelial carcinoma and uncover a novel mechanism by which loss of TGFβ receptor II (Tgfbr2) mediates invasion and metastasis through de-repression of ELMO1, a RAC-activating guanine exchange factor, specifically in cancer stem cells of transition zone tumors. We identify ELMO1 as a novel target of TGFβ signaling and show that restoration of Tgfbr2 results in a complete block of ELMO1 in vivo. Knocking down Elmo1 impairs metastasis of carcinoma cells to the lung, thereby providing insights into the mechanisms of progression of Tgfbr2-deficient invasive transition zone squamous cell carcinoma.