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The JAK-STAT signaling pathway (Janus Kinase / Signal Transducer and Activator of Transcription) is a fundamental intracellular signaling cascade that directly links extracellular cytokines and growth factors to nuclear gene expression.
This pathway plays a central role in immune responses, cell proliferation, differentiation, angiogenesis, and apoptosis. Because of its simplicity and speed – signal transmission from membrane to nucleus – JAK-STAT signaling is essential for rapid cellular responses.
Dysregulation of JAK-STAT signaling is strongly associated with autoimmune diseases, chronic inflammation, cancer, and hematological disorders, making it a major focus in biomedical and translational research.
JAK-STAT pathway activity can be efficiently assessed through targeted gene expression analysis of pathway regulators and downstream transcriptional targets.
JAK-STAT signaling pathway biomarker list
View the genes and molecular targets included in our JAK-STAT pathway qPCR arrays.
Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway. Membrane cytokine receptors have cytoplasmic tails in which inactive JAKs associate constitutively. The interaction of cytokines or growth factors with their receptors (type I and II) induces dimerization/oligomerization of these receptors. It should be mentioned that some cytokine receptors, such as GHR and EpoR, show pre-formed dimers. In both cases, the interaction between the cytokine and its receptor induces a conformational change in the cytoplasmic domain.
This interaction results in the juxtaposition of JAKs, leading to their autophosphorylation or transphosphorylation by other JAKs or other families of tyrosine kinases. The activated JAKs then phosphorylate the receptor’s cytoplasmic tails on tyrosine residues, creating sites that allow the binding of other signaling molecules that contain an SH2 domain (such as STAT proteins). Cytoplasmic STATs then bind to phosphorylated receptors, becoming substrates for JAKs, which phosphorylate STATs on highly conserved tyrosine residues.
After their phosphorylation, STATs form homodimers or heterodimers that are capable of translocating to the nucleus and activating gene transcription. The JAK/STAT pathway is negatively regulated by the suppressors of cytokine signaling (SOCS), as well as by the protein inhibitor of activated STAT (PIAS) and protein tyrosine phosphatases (PTPs).
The JAK family consists of JAK1, JAK2, JAK3, and TYK2, non-receptor tyrosine kinases constitutively associated with cytokine receptors.
STAT proteins (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, STAT6) act as transcription factors activated downstream of JAKs.
Type I and II cytokine receptors lack intrinsic kinase activity and rely on JAKs for signal transduction.
JAK-STAT signaling is tightly regulated by:
Activation begins when cytokines, hormones, or growth factors bind to their receptors, inducing receptor dimerization or conformational changes.
This leads to:
Negative feedback mechanisms prevent excessive or prolonged signaling.
JAK-STAT signaling regulates multiple essential biological processes:
Cancer and tumor progression
Persistent activation of STAT3 and STAT5 promotes tumor cell survival, proliferation, immune evasion, and metastasis in many solid and hematological cancers.
Autoimmune and inflammatory diseases
Aberrant JAK-STAT signaling is implicated in:
Neurological and infectious diseases
JAK-STAT signaling also contributes to:
Because of its central role in disease, JAK-STAT signaling is a major therapeutic target.
At AnyGenes®, we provide high-performance qPCR arrays and customizable SignArrays® designed for JAK-STAT pathway analysis and biomarker discovery.
Our solutions allow researchers to:
What can be analyzed?
Available solutions
Customize your own signaling pathways (SignArrays®) with the factors of your choice!
Simply download and complete our Personalized SignArrays® information file and send it at [email protected] to get started on your project.
The JAK-STAT pathway transmits signals from cytokines and growth factors to the nucleus, regulating gene expression involved in immune responses, cell growth, and survival.
JAK-STAT dysregulation is linked to cancer, autoimmune diseases, chronic inflammation, hematological disorders, and infectious diseases.
JAK inhibitors are used to treat autoimmune and inflammatory diseases and are under investigation for cancer and hematological malignancies.
Ligand binding, receptor dimerization, JAK activation, STAT phosphorylation, STAT dimerization, nuclear translocation, and gene transcription.
By measuring expression levels of pathway regulators and downstream targets using targeted qPCR pathway arrays.
| Signaling Pathways | Product ref | Informations |
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JAK-STAT Signaling Pathway | JAK1H1 |
| Signaling Pathways | Product ref | Informations |
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JAK-STAT Signaling Pathway | JAK1M1 |
| Signaling Pathways | Product ref | Informations |
|---|---|---|
JAK-STAT Signaling Pathway | ******* |
| Signaling Pathways | Product ref | Informations |
|---|---|---|
JAK-STAT Signaling Pathway | ******* |
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