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. 2020 May 25;18:78. doi: 10.1186/s12964-020-00547-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — Schematic diagram illustrating the different in canonical versus non-canonical response to IL-12. a The canonical IL-12 pathway is triggered by (1) ligand-mediated heterodimerization of the receptor subunits IL12RB1 and IL12RB2. (2) Formation of the receptor complex promotes the phosphorylation of receptor associated kinases JAK2 and TYK2 and of a signal transducer binding site on the cytoplasmic tail of IL12RB2. (3) Phosphorylation of this IL12RB2 binding site attracts STAT4 that is subsequently phosphorylated by JAK2. (4) Phosphorylated STAT4 dimerizes and translocates into the nucleus to initiate STAT4-mediated transcription that promotes cell proliferation and Interferon-gamma production. b The non-canonical IL-12 pathway is triggered by (1) IL-12-enhanced homodimerization of IL12RB2 subunits. (2) Homodimerization of IL12RB2 activates the JAK2 receptor associated kinases, which in turn (3) recruit and activate PI3K via the p85a subunit. (4) Activated PI3K then phosphorylates Thr308-primed Akt at the Ser 472/473 loci, which engages the canonical Akt response that includes enhanced survival