Cell Signaling Technology

Phospho-Jak2 (Tyr1007/1008) Antibody

#3771 · $362

100
Citing papers
14.4k
Combined citations
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Research areas

Pain Mechanisms and Treatments11Cancer Immunotherapy and Biomarkers10Immune cells in cancer10Neuroscience and Neuropharmacology Research7Immune Response and Inflammation6Cytokine Signaling Pathways and Interactions6Neurogenesis and neuroplasticity mechanisms6MicroRNA in disease regulation6

Papers citing this product

1
JNK-Induced MCP-1 Production in Spinal Cord Astrocytes Contributes to Central Sensitization and Neuropathic Pain
Journal of Neuroscience·2009·564 cit.·DOI
2
Shifts in macrophage phenotypes and macrophage competition for arginine metabolism affect the severity of muscle pathology in muscular dystrophy
Human Molecular Genetics·2008·510 cit.·DOI
3
Epigenetic regulation of the alternatively activated macrophage phenotype
Blood·2009·491 cit.·DOI
4
An ESRP‐regulated splicing programme is abrogated during the epithelial–mesenchymal transition
The EMBO Journal·2010·386 cit.·DOI
5
Ionotropic and Metabotropic Receptors, Protein Kinase A, Protein Kinase C, and Src Contribute to C-Fiber-Induced ERK Activation and cAMP Response Element-Binding Protein Phosphorylation in Dorsal Horn Neurons, Leading to Central Sensitization
Journal of Neuroscience·2004·377 cit.·DOI
6
Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency
Molecular Cell·2021·315 cit.·DOI
7
BRCA locus-specific loss of heterozygosity in germline BRCA1 and BRCA2 carriers
Nature Communications·2017·308 cit.·DOI
8
Melanoma cell-secreted exosomal miR-155-5p induce proangiogenic switch of cancer-associated fibroblasts via SOCS1/JAK2/STAT3 signaling pathway
Journal of Experimental & Clinical Cancer Research·2018·290 cit.·DOI
9
Enhanced Immunosuppressive Properties of Human Mesenchymal Stem Cells Primed by Interferon-γ
EBioMedicine·2018·285 cit.·DOI
10
The tale of TILs in breast cancer: A report from The International Immuno-Oncology Biomarker Working Group
npj Breast Cancer·2021·269 cit.·DOI

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