Related Experiment Video
Updated: May 18, 2026

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
Published on: March 9, 2012
RAC1 in keratinocytes regulates crosstalk to immune cells by Arp2/3-dependent control of STAT1
Esben Pedersen1, Zhipeng Wang, Alanna Stanley
1Biomedical Institute, BRIC, University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen, Denmark.
Abstract:
Crosstalk between keratinocytes and immune cells is crucial for the immunological barrier function of the skin, and aberrant crosstalk contributes to inflammatory skin diseases. Using mice with a keratinocyte-restricted deletion of the RAC1 gene we found that RAC1 in keratinocytes plays an important role in modulating the interferon (IFN) response in skin. These RAC1 mutant mice showed increased sensitivity in an irritant contact dermatitis model, abnormal keratinocyte differentiation, and increased expression of immune response genes including the IFN signal transducer STAT1. Loss of RAC1 in keratinocytes decreased actin polymerization in vivo and in vitro and caused Arp2/3-dependent expression of STAT1, increased interferon sensitivity and upregulation of aberrant keratinocyte differentiation markers. This can be inhibited by the AP-1 inhibitor tanshinone IIA. Loss of RAC1 makes keratinocytes hypersensitive to inflammatory stimuli both in vitro and in vivo, suggesting a major role for RAC1 in regulating the crosstalk between the epidermis and the immune system.
Related Concept Videos
The JAK-STAT Signaling Pathway
MAPK Signaling Cascades
Intracellular Signaling Affects Focal Adhesions
Some...
The Ras Gene
Ras is a superfamily...
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Cytoskeletal Coordination in Cell Migration
