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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
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IL1RAP potentiates multiple oncogenic signaling pathways in AML.

Kelly Mitchell1, Laura Barreyro1, Tihomira I Todorova1

  • 1Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY.

The Journal of Experimental Medicine
|May 19, 2018
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Targeting interleukin-1 receptor accessory protein (IL1RAP) inhibits acute myeloid leukemia (AML) growth by interacting with FLT3 and c-KIT. This approach shows promise for AML therapy without harming healthy blood cells.

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Area of Science:

  • Hematology
  • Molecular Biology
  • Cancer Research

Background:

  • Interleukin-1 receptor accessory protein (IL1RAP) is overexpressed in acute myeloid leukemia (AML) and other myeloid malignancies.
  • IL1RAP is a potential therapeutic target, but its cell-intrinsic functions in AML are not well understood.

Purpose of the Study:

  • To investigate the cell-intrinsic functions of IL1RAP in AML pathogenesis.
  • To explore the therapeutic potential of targeting IL1RAP in AML.

Main Methods:

  • Targeting IL1RAP using RNA interference, genetic deletion, and antibodies.
  • In vitro and in vivo studies in AML models.
  • Investigating IL1RAP interactions with FLT3 and c-KIT receptor tyrosine kinases.

Main Results:

  • Targeting IL1RAP inhibited AML progression in vitro and in vivo.
  • Therapeutic targeting of IL1RAP did not affect healthy hematopoietic function or viability.
  • IL1RAP interacts with FLT3 and c-KIT, mediating signaling and proliferation in AML.

Conclusions:

  • IL1RAP plays a critical role in AML pathogenesis beyond the IL-1 receptor pathway.
  • Targeting IL1RAP offers a promising therapeutic strategy for AML with a favorable safety profile.
  • The interaction of IL1RAP with FLT3 and c-KIT provides a new mechanistic understanding of its role in AML.