In 2018 Xu et al. showed that WDR62 stability and neurogenesis is regulated by MEKK3 in coordination with FBW7 (F-box and WD repeat domain-containing protein 7).[9]
Prinz et al. showed a significant role for WDR62 in mediating activation of the JNK pathway in response to TNFα. This finding might have implication in the research of TNFα related diseases such as autoimmune diseases and cancer. [10]
In 2020 Shohayeb et al. revealed a relationship between the cortical malformation, associated with WDR62 point mutations occurring in humans (V65M and R438H), and ciliopathies. These WDR62 point mutations drive ciliary disruption in Radial glial cell via disrupting the cilia and centrosome localization of CENPJ and the Intraflagellar transport protein 88 (IFT88), which are required for tubulin requitment to centrosome and transport of tubulin to the cilia tip, respectively.[11]
^Shohayeb, B, et al. (January 2020). "The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development". HMG. 29 (2): 248–263. doi:10.1093/hmg/ddz281. PMID31816041.
Rual JF, Venkatesan K, Hao T, et al. (2005). "Towards a proteome-scale map of the human protein-protein interaction network". Nature. 437 (7062): 1173–8. doi:10.1038/nature04209. PMID16189514.