{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSTAT5A is a pivotal transcription factor activated upon tyrosine‐phosphorylation by a wide spectrum of extracellular signals—including hormones, receptor tyrosine kinases, and cytokine receptors—that modulate its nuclear translocation and transcriptional activity. In mammary epithelial cells, for example, prolactin‐induced STAT5A activation (accompanied by specific posttranslational modifications such as O‐GlcNAc glycosylation that are essential for high‐order oligomer formation) drives the transcription of key differentiation and cell‐cycle regulators (e.g. cyclin D1) and cooperates with ERBB4 intracellular domains to direct milk gene expression. Moreover, NF‑κB signals can positively regulate STAT5A gene expression in certain lymphoid malignancies, underscoring how receptor‐proximal events are relayed to nuclear transcriptional programs."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn hematopoietic and immune cell contexts, STAT5A activation is critical for cell survival, self‐renewal, and differentiation. Constitutive activation of STAT5A (often driven by oncogenic fusion kinases such as BCR–ABL) is a key mediator in chronic myelogenous leukemia and acute lymphoblastic leukemia, where its dimer–tetramer equilibrium as well as its engagement with cytoplasmic effectors like PI3‑kinase and Akt contribute both to malignant cell proliferation and resistance to tyrosine kinase inhibitors. In addition, STAT5A functions downstream of receptors such as those for IL‑2, IL‑15, TSLP, and even leptin; these signals ultimately modulate immune responses by inducing FOXP3 expression in activated T cells or by regulating other cytokine genes, while also impacting normal hematopoietic progenitor self‐renewal and erythroid differentiation. Thus, tight regulation of STAT5A activity—via its phosphorylation status, oligomerization dynamics, and even epigenetic control—is critical for maintaining normal immune homeostasis and hematopoiesis, whereas its dysregulation contributes to leukemogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn solid tumors and endocrine tissues, STAT5A exhibits context‐dependent roles that can be either tumor‐promoting or –suppressive. In breast and prostate cancers, active STAT5A has been linked to enhanced differentiation and a more favorable prognosis by promoting cell‐cycle regulation and adhesion molecule expression; however, in other settings, its activity may drive invasive behavior, metastasis, or resistance to therapy via cross‐talk with hormone receptors (such as the androgen receptor) and by modulating transcription of genes including BCL6. Nuclear complexes comprising STAT5A and growth factor receptors (for example, FGFR‑2) have also been observed, suggesting that STAT5A can function as a coactivator within transcriptional regulatory networks. Moreover, STAT5A can be co‐opted by viral oncogenes (e.g. HPV E7) and participate in noncanonical cytoplasmic signaling in megakaryocytes, further underscoring its multifaceted functions in normal tissue homeostasis and tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "35"}, {"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jennifer L Brockman, Matthew D Schroeder, Linda A Schuler "}, {"type": "b", "children": [{"type": "t", "text": "PRL activates the cyclin D1 promoter via the Jak2/Stat pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Endocrinol (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1210/mend.16.4.0817"}], "href": "https://doi.org/10.1210/mend.16.4.0817"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "11923474"}], "href": "https://pubmed.ncbi.nlm.nih.gov/11923474"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Michael Hinz, Petra Lemke, Ioannis Anagnostopoulos, et al. 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