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. 2020 Feb 18;9(2):25. doi: 10.1038/s41389-020-0210-7

Fig. 6. Model for HELLS function as driver of tumorigenesis in the developing retina.

Fig. 6

a In the normal developing retina, RB or p107 represses E2F1 from driving HELLS expression by postnatal day 6 (P6). b In the absence of RB and p107, E2F1 drives Hells transcription beyond of P6. HELLS is known to interact physically with E2F3 and function as transcriptional co-activator of E2F3. The resulting HELLS overexpression in the absence of RB and p107 mediate expression of several genes that stimulate G1/S transition and cell proliferation.