Copg1, a subunit of the coatomer complex I (COPI), is involved in mediating retrograde vesicular trafficking from Golgi to the endoplasmic reticulum (ER) and within Golgi compartments [1]. COPI is crucial for maintaining the proper organization and function of the Golgi apparatus and ER, which are key cellular components involved in protein processing and transport.

Genetic deletion of COPG1 in in vitro models leads to aberrant activation of the STING pathway and type I IFN activation, suggesting its role in innate immune regulation [1]. In a proteome-wide association study, COPG1 was associated with an increased risk of breast cancer, indicating its potential involvement in cancer-related biological processes [2]. A new severe congenital neutropenia syndrome, caused by autosomal recessive COPZ1 mutations, showed that these mutations affected the interaction with COPG1 and led to impaired granulocytic differentiation, highlighting COPG1's importance in hematopoiesis [3].

In summary, Copg1 plays essential roles in vesicular trafficking, innate immune response, hematopoiesis, and may be associated with breast cancer development. Studies using genetic deletion in in vitro models have been instrumental in revealing these functions, providing insights into the biological processes and disease conditions related to Copg1.