RMP1-14 is specific clone name for a rat anti-mouse PD-1 antibody. The original hybridoma was generated by immunizing Sprague Dawley rats with mouse PD-1-transfected BHK cells. A P3U1 myeloma was used as the fusion partner.
Who was it created by?
It was developed by Professor Hideo Yagita at the Juntendo University School of Medicine
Where was it first published?
Authors: Yamazaki et al.
Journal Title: Blockade of B7-H1 on macrophages suppresses CD4+ T cell proliferation by augmenting IFN-gamma-induced nitric oxide production.
Journal: J Immunol.
Additonal Info: 2005 Aug 1;175(3):1586-92 PMID:16034097
The article above describes the generation and initial characterisation of the RMP1-14 hybridoma
Like the J43 clone, RMP1-14 has been shown to block the binding of both mouse PD-L1-Ig and mouse PD-L2-Ig to PD-1.
A total of 470 articles have been published over the last three years citing RMP1-14, with scientists from 300 organisations in 32 countries contributing to the research. The top authors publishing articles using RMP1-14 in the last three years are show in Table 1 below.
Table 1: The top 10 most prolific authors citing RMP1-14 in the last 3 years
A breakdown of the main locations of the authors are shown in Image 1 and 2 below. In Image 3 we show the main journals that cite work using RMP1-14.
Image 1: Citations by Country
Image 2: Citations by State (USA)
Image 3: Citations by Journal
Images kindly provided by SciLeads
Latest Research Articles Using RMP1-14
- Tristan Rupp, Porsolt SAS. Anti-CTLA-4 and anti-PD-1 immunotherapies repress tumor progression in preclinical breast and colon model with independent regulatory T cells response.
- Jianxin Wang, John Hopkins University School of Medicine. CCR2/CCR5 inhibitor permits the radiation-induced effector T cell infiltration in pancreatic adenocarcinoma.
- Atsushi Enomoto, Nagoya University. Meflin-positive cancer-associated fibroblasts enhance tumor response to immune checkpoint blockade.
- Robert Sobol, Multivir. Tumor suppressor immune gene therapy to reverse immunotherapy resistance.