Kbtbd11, Kelch repeat and BTB domain-containing protein 11, is involved in multiple biological processes. It is associated with adipogenesis, osteoclastogenesis, and may play a role in tumorigenesis. In adipocytes, it may be part of pathways related to adipocyte differentiation and homeostasis, and in osteoclasts, it is involved in the regulation of osteoclast differentiation pathway [1,2,3,4].

In adipocyte-related functional studies, knockdown of Kbtbd11 in 3T3-L1 cells suppressed adipogenesis, while overexpression promoted it. Its mRNA levels increase during 3T3-L1 differentiation, and are affected by feeding states in mice, with higher levels in re-fed and diet-induced obese mice. Also, PPARγ acts on the Kbtbd11 gene region to regulate its expression, and it interacts with HSC70 and HSP60 to regulate NFATc1 proteolysis. In osteoclasts, knockdown of Kbtbd11 enhanced osteoclast formation and increased osteoclast marker genes expression, while overexpression impaired osteoclast differentiation. Kbtbd11 interacts with Cullin3 to promote ubiquitination and degradation of NFATc1, a key factor for osteoclast differentiation [1,2,3,4].

In conclusion, Kbtbd11 is essential for adipocyte differentiation and osteoclast regulation. Studies using gene knockdown (a form of in-vivo loss-of-function model) in cell lines like 3T3-L1 and in understanding osteoclastogenesis have revealed its role. These findings suggest its potential as a therapeutic target in obesity and perhaps in bone-related diseases where osteoclast activity needs regulation [1,2,3,4].