Cell Signaling Technology

PKR (D7F7) Rabbit Monoclonal Antibody

#12297 · $174

100
Citing papers
13.5k
Combined citations
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Research areas

Autophagy in Disease and Therapy31Cancer Immunotherapy and Biomarkers22Immunotherapy and Immune Responses12Endoplasmic Reticulum Stress and Disease9Immune Cell Function and Interaction7Nerve injury and regeneration7CAR-T cell therapy research6Ubiquitin and proteasome pathways6

Papers citing this product

1
PD-L1 regulates the development, maintenance, and function of induced regulatory T cells
The Journal of Experimental Medicine·2009·2k cit.·DOI
2
Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma
Blood·2010·1.3k cit.·DOI
3
ProBDNF Induces Neuronal Apoptosis via Activation of a Receptor Complex of p75<sup>NTR</sup>and Sortilin
Journal of Neuroscience·2005·991 cit.·DOI
4
Host expression of PD-L1 determines efficacy of PD-L1 pathway blockade–mediated tumor regression
Journal of Clinical Investigation·2018·598 cit.·DOI
5
Plasma cells from multiple myeloma patients express B7-H1 (PD-L1) and increase expression after stimulation with IFN-γ and TLR ligands via a MyD88-, TRAF6-, and MEK-dependent pathway
Blood·2007·575 cit.·DOI
6
Pharmacological Inhibition of ULK1 Kinase Blocks Mammalian Target of Rapamycin (mTOR)-dependent Autophagy
Journal of Biological Chemistry·2015·374 cit.·DOI
7
Hypoxia ameliorates intestinal inflammation through NLRP3/mTOR downregulation and autophagy activation
Nature Communications·2017·312 cit.·DOI
8
PD-1 mediates functional exhaustion of activated NK cells in patients with Kaposi sarcoma
Oncotarget·2016·291 cit.·DOI
9
Characterization of PF-4708671, a novel and highly specific inhibitor of p70 ribosomal S6 kinase (S6K1)
Biochemical Journal·2010·267 cit.·DOI
10
Tumor-secreted Pros1 inhibits macrophage M1 polarization to reduce antitumor immune response
Journal of Clinical Investigation·2018·213 cit.·DOI

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