Zfp251, a member of the C2H2 ZFP family with a Krüppel-associated box domain, mainly acts as a transcriptional repressor. Its cellular function has been explored through genetic models. It may be involved in multiple biological processes such as adipocyte-related metabolism and hematopoietic stem cell regulation [1,2].

In a gene-knockout-like study, Zfp251 deficiency in mice led to glucose intolerance due to impaired insulin signaling caused by white adipose tissue (WAT) hypertrophy. Gene ontology analysis showed it affected genes related to adipocyte differentiation and lipid metabolism. In vitro, Zfp251 knockdown in 3T3-L1 adipocytes led to hypertrophic changes, and in pre-adipocytes, it caused cell cycle arrest in G0/G1 phase, impairing adipocyte differentiation [1]. Also, a functional screen identified Zfp251 as one of 17 regulators of murine hematopoietic stem cell (HSC) repopulation, with its knockdown resulting in a loss of function [2].

In summary, Zfp251 plays a crucial role in adipocyte-related glucose metabolism and hematopoietic stem cell repopulation. The use of Zfp251-deficient mouse models has revealed its importance in these biological processes, which may have implications for understanding metabolic and hematopoietic-related diseases.

References:

1. Kim, Eunsu, Ham, Sun Ah, Hwang, Jung Seok, Hur, Jinwoo, Seo, Han Geuk. 2022. Zinc finger protein 251 deficiency impairs glucose metabolism by inducing adipocyte hypertrophy. In Molecular and cellular endocrinology, 562, 111838. doi:10.1016/j.mce.2022.111838. https://pubmed.ncbi.nlm.nih.gov/36565788/

2. Holmfeldt, Per, Ganuza, Miguel, Marathe, Himangi, Tan, Kai, McKinney-Freeman, Shannon. 2016. Functional screen identifies regulators of murine hematopoietic stem cell repopulation. In The Journal of experimental medicine, 213, 433-49. doi:10.1084/jem.20150806. https://pubmed.ncbi.nlm.nih.gov/26880577/