Magic™ Anti-STAT3 monoclonal antibody (DCABH-9701)

Rabbit Anti-Human STAT3 (Phospho Y705) monoclonal antibody for WB, IP, IHC-P, ICC

Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Clone
FQ3258Z
Species Reactivity
Mouse, Rat, Human
Immunogen
A synthetic phospho-peptide corresponding to residues surrounding tyrosine 705 of human STAT3.
Conjugate
Unconjugated

Applications


Application Notes
WB: 1/200000; IP: 1/20; IHC-P: 1/50 - 1/100; ICC/IF: 1/100
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
STAT3; signal transducer and activator of transcription 3 (acute-phase response factor); signal transducer and activator of transcription 3; APRF; DNA-binding protein APRF; acute-phase response factor
Entrez Gene ID
UniProt ID

Product Background


Pathway
Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem; Adipogenesis, organism-specific biosystem; Androgen Receptor Signaling Pathway, organism-specific biosystem; B Cell Receptor Signaling Pathway, organism-specific biosystem;

Citations


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Custom Antibody Labeling


We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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References


Response to radiotherapy in pancreatic ductal adenocarcinoma is enhanced by inhibition of myeloid-derived suppressor cells using STAT3 anti-sense oligonucleotide

CANCER IMMUNOLOGY IMMUNOTHERAPY

Authors: Oweida, Ayman J.; Mueller, Adam C.; Piper, Miles; Milner, Dallin; Van Court, Benjamin; Bhatia, Shilpa; Phan, Andy; Bickett, Thomas; Jordan, Kimberly; Proia, Theresa; Schulick, Richard; Messersmith, Wells A.; Del Chiaro, Marco; Clambey, Eric; Gough, Michael J.; Williams, Jason; Hansen, Kirk; Goodman, Karyn; Karam, Sana D.

Pancreatic ductal adenocarcinoma (PDAC) has a heterogeneous tumor microenvironment (TME) comprised of myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages, neutrophils, regulatory T cells, and myofibroblasts. The precise mechanisms that regulate the composition of the TME and how they contribute to radiotherapy (RT) response remain poorly understood. In this study, we analyze changes in immune cell populations and circulating chemokines in patient samples and animal models of pancreatic cancer to characterize the immune response to radiotherapy. Further, we identify STAT3 as a key mediator of immunosuppression post-RT. We found granulocytic MDSCs (G-MDSCs) and neutrophils to be increased in response to RT in murine and human PDAC samples. We also found that RT-induced STAT3 phosphorylation correlated with increased MDSC infiltration and proliferation. Targeting STAT3 using an anti-sense oligonucleotide in combination with RT circumvented RT-induced MDSC infiltration, enhanced the proportion of effector T cells, and improved response to RT. In addition, STAT3 inhibition contributed to the remodeling of the PDAC extracellular matrix when combined with RT, resulting in decreased collagen deposition and fibrotic tissue formation. Collectively, our data provide evidence that targeting STAT3 in combination with RT can mitigate the pro-tumorigenic effects of RT and improve tumor response.

The CDK4/6-EZH2 pathway is a potential therapeutic target for psoriasis

JOURNAL OF CLINICAL INVESTIGATION

Authors: Mueller, Anne; Dickmanns, Antje; Resch, Claudia; Schaekel, Knut; Hailfinger, Stephan; Dobbelstein, Matthias; Schulze-Osthoff, Klaus; Kramer, Daniela

Psoriasis is a frequent, inflammatory skin disease characterized by keratinocyte hyperproliferation and a disease-related infiltration of immune cells. Here, we identified a novel proinflammatory signaling pathway driven by cyclin-dependent kinase 4 (CDK4) and CDK6 and the methyltransferase EZH2 as a valid target for psoriasis therapy. Delineation of the pathway revealed that CDK4/6 phosphorylated EZH2 in keratinocytes, thereby triggering a methylation-induced activation of STAT3. Subsequently, active STAT3 resulted in the induction of I kappa B zeta which is a key proinflammatory transcription factor required for cytokine synthesis in psoriasis. Pharmacological or genetic inhibition of CDK4/6 or EZH2 abrogated psoriasis-related proinflammatory gene expression by suppressing I kappa B zeta induction in keratinocytes. Importantly, topical application of CDK4/6 or EZH2 inhibitors on the skin was sufficient to fully prevent the development of psoriasis in various mouse models by suppressing STAT3-mediated I kappa B zeta expression. Moreover, we found a hyperactivation of the CDK4/6-EZH2 pathway in human and mouse psoriatic skin lesions. Thus, this study not only identifies a novel psoriasis-relevant proinflammatory pathway, but also proposes the repurposing of CDK4/6 or EZH2 inhibitors as a new therapeutic option for patients with psoriasis.

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