Cytokines play critical roles in the regulation of embryonic stem cells (ESCs), the pluripotent cells with the ability to differentiate into all cell types of the body. Cytokines mediate communication between cells in the embryonic microenvironment, influencing ESC self-renewal, differentiation, and maintenance of pluripotency. Several cytokines and their signalling pathways have been identified as key players in ESC biology. Leukaemia Inhibitory Factor (LIF) is the key cytokine that helps maintain pluripotency in mouse ESCs (mESCs). LIF activates the JAK/STAT signalling pathway by binding to its receptor, leading to the phosphorylation and activation of STAT3 (Signal Transducer and Activator of Transcription 3). Activated STAT3 translocates to the nucleus promoting the expression of pluripotency-related genes such as Oct4, Nanog, and Sox2. This, in turn, maintains the undifferentiated state of mESCs. LIF/STAT3 signalling is critical for the self-renewal and pluripotency of mESCs and is often used in vitro to support their maintenance in gene targeting studies. LIF/STAT3 is however dispensable for maintenance of human ES cells. IL-6 is another cytokine that activates the JAK/STAT3 pathway. Like LIF, IL-6 can also support mESC self-renewal and pluripotency. IL-6 signalling, along with other factors, helps maintain mESC cultures without the need for a feeder cell layer expressing these factors. In addition to LIF, Fibroblast Growth Factors (FGFs) including FGF2 and FGF4, play a role in maintaining pluripotency and self-renewal in both mouse and human ESCs (hESCs). FGFs activate the MAPK/ERK signalling pathway, which can promote differentiation. However, in the presence of LIF or other self-renewal factors, FGF signalling helps maintain ESC pluripotency. The balance between FGF and LIF signalling is critical for ESC fate decisions, with high FGF and low LIF promoting differentiation and vice versa. Bone Morphogenetic Proteins (BMPs) are members of the transforming growth factor-beta (TGF-β) superfamily and play dual roles in ESCs. In mESCs, BMP signalling induces differentiation by phosphorylating SMAD1/5/8 and promoting the expression of differentiation-associated genes. However, in contrast, BMP4 can have an opposite effect on hESCs when combined with FGF2, helping to maintain pluripotency. Thus, the precise role of BMP signalling in ESCs depends on context and other culture conditions. Nodal and Activin are also TGF-β superfamily members that activate SMAD2/3 signalling in ESCs. In hESCs, Nodal/Activin signalling is essential for maintaining hESC pluripotency, activating a SMAD2/3-Oct4/Nanog/Sox2 pathway that supports self-renewal. In mouse development, Nodal signalling plays a critical role in the establishment of the pluripotent epiblast during early embryogenesis. Wnt signalling is also involved in ESC self-renewal and differentiation. It can activate both the canonical (β-catenin-dependent) and non-canonical (β-catenin-independent) pathways. Low-level Wnt signalling can promote self-renewal by stabilizing β-catenin, which interacts with TCF/LEF transcription factors and regulates pluripotency genes. However, excessive Wnt signalling can also lead to differentiation by activating target genes involved in lineage commitment. Finally, TGF-β family members, such as TGF-β1, TGF-β2, and Growth Differentiation Factor 3 (GDF3), have varying effects on ESCs. TGF-β1 promotes differentiation in mESCs, whilst GDF3 can enhance self-renewal and pluripotency in both mESCs and hESCs. We offer a wide product catalogue of research tools for investigating cytokines, including IRF6 antibodies. Explore our full cytokines product range below and discover more, for less.