STAT5
STAT5 comprises STAT5A and STAT5B, transcription factors that regulate hematopoietic cell proliferation, differentiation, and apoptosis[1]. Mechanistically, STAT5 tyrosine phosphorylation in peripheral T cells is driven by cytokine receptor signaling rather than the T-cell receptor complex[2]. This cytokine-linked pathway supports immune regulation, lymphocyte development, and cell survival programs[3]. In disease contexts, STAT5B deficiency is associated with growth failure, immunodeficiency, and severe pulmonary disease[4]. Compared with STAT5A, STAT5B shows dominant activity in effector and regulatory T-cell responses, with paralog dose explaining much functional specificity[5]. In BCR/ABL leukemia models, STAT5B, but not STAT5A, serves as the major STAT5 isoform driving leukemogenesis[6]. For experimental applications, AC-4-130 directly binds STAT5 and disrupts activation, dimerization, nuclear translocation, and STAT5-dependent transcription in AML models[7]. Pimozide also decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors[8].
References:
- [1]. Nosaka T, et al. STAT5 as a molecular regulator of proliferation, differentiation and apoptosis in hematopoietic cells. EMBO J. 1999 Sep 1;18(17):4754-65. [Content Brief]
- [2]. Moriggl R, et al. Stat5 activation is uniquely associated with cytokine signaling in peripheral T cells. Immunity. 1999 Aug;11(2):225-30. [Content Brief]
- [3]. Smith MR, et al. STAT5b: A master regulator of key biological pathways. Front Immunol. 2023 Jan 23;13:1025373. [Content Brief]
- [4]. Nadeau K, et al. STAT5b deficiency: an unsuspected cause of growth failure, immunodeficiency, and severe pulmonary disease. J Pediatr. 2011 May;158(5):701-8. [Content Brief]
- [5]. Villarino A, et al. Signal transducer and activator of transcription 5 (STAT5) paralog dose governs T cell effector and regulatory functions. Elife. 2016 Mar 21;5:e08384. [Content Brief]
- [6]. Kollmann S, et al. Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia. Leukemia. 2019 Jul;33(7):1583-1597. [Content Brief]
- [7]. Wingelhofer B, et al. Pharmacologic inhibition of STAT5 in acute myeloid leukemia. Leukemia. 2018 May;32(5):1135-1146. [Content Brief]
- [8]. Nelson EA, et al. The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors. Blood. 2011 Mar 24;117(12):3421-9. [Content Brief]
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STAT5 Related Products (66)
Related Products (66)
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Antibodies (5)
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Geranylgeranyl pyrophosphate
0 ImagesGeranylgeranyl pyrophosphate is a type of isoprenoid metabolic intermediate, mainly synthesized through the mevalonate pathway. Geranylgeranyl pyrophosphate is a key precursor in various biological synthesis processes, especially as a necessary substrate for post-translational modification of proteins - geranylgeranyl phosphorylation. Geranylgeranyl pyrophosphate regulates various cellular processes and disease progression through protein geranylgeranyl phosphorylation, such as activating the YAP signaling pathway, promoting cell proliferation and inhibiting apoptosis; promoting IL-2 production and STAT5 phosphorylation; and influencing metabolic homeostasis and cancer, etc.
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FI-700
0 ImagesCat. No.: HY-111268CAS No.: 866883-79-6FI-700 is an orally active FLT3 inhibitor with an IC50 of 20 nM. FI-700 induces G1 phase cell cycle arrest by inhibiting autophosphorylation of mutant FLT3 and the downstream STAT5/MAPK pathway. FI-700 triggers the mitochondrial apoptosis pathway by downregulating anti-apoptotic proteins Mcl-1 and Bcl-XL, altering the conformation of Bax, and activating caspase-3. FI-700 can be used in research related to acute myeloid leukemia.
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CHMFL-48
0 ImagesCat. No.: HY-164469CAS No.: 2479290-65-6CHMFL-48 is an orally active BCR-ABL kinase inhibitor targeting both wild-type (wt) and various imatinib-resistant mutants. The IC50 values for CHMFL-48 against ABL wild-type and ABL T315I mutant are 1 nM and 0.8 nM, respectively. CHMFL-48 exerts its effects by blocking the autophosphorylation of BCR-ABL wild-type and mutant forms, which impacts downstream signaling mediators such as STAT5 and CRKL, leading to cell cycle arrest and induction of apoptosis. CHMFL-48 holds potential for research into chronic myeloid leukemia (CML).
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MK256
0 ImagesCat. No.: HY-183423CAS No.: 2271348-04-8MK256 is an orally active, selective CDK8 inhibitor and CDK19/cyclin C inhibitor with IC50 values of 2.5 nM and 3.3 nM, respectively. MK256 downregulates phosphorylated STAT1 (S727), STAT5 (S726), MCL-1 mRNA and CCL2 mRNA. MK256 exhibits anti-tumor activity in acute myeloid leukemia. MK256 can be used for the research of acute myeloid leukemia.
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CT 2576
0 ImagesCat. No.: HY-187609CAS No.: 166981-11-9CT 2576 is a phospholipid signaling inhibitor as well as a Jak3/STAT5 inhibitor. CT 2576 suppresses gene expression and replication of human immunodeficiency virus (HIV) at the post-transcriptional level by interfering with phospholipid metabolism in host cells, particularly by inhibiting the production of phosphatidic acid PA. CT-2576 completely inhibits the growth and proliferation of malignant T-cell lymphoma cells by suppressing phospholipid signaling and blocking the Jak/STAT signaling pathway associated with IL-2R. CT 2576 can be used in research related to human immunodeficiency virus (HIV) infection and cutaneous T-cell lymphoma (CTCL).
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BP-1-108
0 ImagesCat. No.: HY-125151CAS No.: 1334492-85-1BP-1-108 is a selective inhibitor of STAT5 (Ki=8.3 μM) with anticancer activity. BP-1-108 induces apoptosis of leukemia cells by inhibiting the phosphorylation of STAT5. BP-1-108 can be used in the study of acute myeloid leukemia and prostate cancer.
