The Transforming Growth Factor-Beta (TGF-β) signalling pathway plays diverse and context-dependent roles in the regulation of self-renewal and differentiation of various types of stem cells. The TGF-β signalling pathway operates through a network of molecular events with TGF-β ligands (TGF-β1, TGF-β2, TGF-β3) binding to specific cell surface receptors (TGF-βRI and TGF-βRII), leading to the phosphorylation and activation of intracellular Smad proteins. Activated Smads then translocate to the nucleus and regulate the transcription of target genes involved in self-renewal, differentiation, and tissue homeostasis. TGF-β signalling is involved in the regulation of ESC pluripotency and differentiation. In the pluripotent state, TGF-β acts to maintain the self-renewal of ESCs by promoting the expression of pluripotency factors like Oct4 and Nanog. However, when ESCs are subjected to differentiation cues, TGF-β can also facilitate their transition into various lineages by modulating the expression of lineage-specific genes. This dual role indicates the context-dependent nature of TGF-β signalling in ESCs. As with ESCs, TGF-β signalling also plays a role in iPSC generation and maintenance. Activation of TGF-β signalling can enhance reprogramming efficiency, as it helps maintain the pluripotent state during the reprogramming process. Conversely, inhibiting TGF-β signalling can promote differentiation and increase the yield of some iPSC-derived differentiated cells. The TGF-β pathway has been extensively studied in the regulation of adult stem cells in various tissues. In some cases, TGF-β signalling promotes stem cell self-renewal and maintenance. For instance, in the hematopoietic system, TGF-β helps maintain the quiescent state of hematopoietic stem cells (HSCs) and prevents their premature differentiation. In the mammary gland, TGF-β similarly supports the self-renewal of mammary stem cells. TGF-β signalling in mammary gland can help maintain mammary stem cells in a quiescent or dormant state, preserving the stem cell pool and preventing their differentiation. However, in other contexts, TGF-β signalling can drive stem cell differentiation. For example, in skeletal muscle, TGF-β signalling promotes the differentiation of muscle satellite cells into myoblasts. In the intestinal epithelium, TGF-β acts as a positive regulator of intestinal stem cell (ISC) differentiation, facilitating the formation of various cell types within the intestinal lining. Dysregulation of the TGF-β pathway is often associated with cancer progression, including the behaviour of cancer stem cells (CSCs). In some cases, TGF-β signalling in CSCs can promote self-renewal, tumour initiation, and progression. For example, in some breast cancer subtypes, TGF-β signalling has been implicated in promoting CSC self-renewal. It can contribute to the maintenance and expansion of the CSC population, which is associated with tumour initiation, progression, and therapy resistance. However, in other instances, it may facilitate differentiation, leading to reduced CSC activity. The precise role of TGF-β signalling in CSCs can therefore vary depending on the tumour type and microenvironment. We provide a wide product catalogue of research reagents for investigating the TGF beta signalling pathway, including Interferon gamma antibodies, c-Myc antibodies, Smad4 antibodies, Interferon gamma ELISA Kits, and Smad3 ELISA Kits. Explore our full TGF beta signalling pathway product range below and discover more, for less. Alternatively, you can explore our Cytoplasmic, Secreted, and Interferon gamma product ranges.