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. 2015 Jul 26;11:919–943. doi: 10.1007/s12015-015-9611-y

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© The Author(s) 2015

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 3 — A hypothetical HIF-1α/2α-dependent signaling crosstalk within putative renal CSCs involving pathways of three associated markers: CD105, CXCR-4 and ALDH. As a presumable oncogene, HIF-2α is supposed to drive progression of pVHL-defective, pseudo-hypoxic ccRCC (the absolute majority of clinical cases), possibly including promotion of aggressive, immature CSC-like phenotype. The figure does not represent pathways in a particular putative renal CSC population, but serves as the summary model of all known interactions in various identified populations. A few complements in signaling crosstalk were taken from [25, 168]