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This study explores the molecular mechanisms underlying variable therapeutic responses to tofacitinib in patients with rheumatoid arthritis (RA). Peripheral blood mononuclear cells (PBMCs) were collected from patients with active RA before tofacitinib treatment. Based on EULAR DAS28-defined clinical...
ORGANISM(S): Homo sapiens 
The myeloma bone marrow microenvironment drives proliferation of malignant plasma cells and promotes resistance to therapy. Interleukin-6 (IL-6) and downstream JAK/STAT signaling are thought to be central components of these microenvironment-induced phenotypes. In a prior drug repurposing screen, we...
ORGANISM(S): Homo sapiens (Human) 
2018-10-24 | PXD006581 | Pride
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease, characterized by synovial hyperplasia and progressive joint destruction. For treating inflammatory diseases, such as RA, the Janus kinase (JAK)-mediated signaling pathway has emerged as a therapeutic target. Therefore, JAK inhib...
ORGANISM(S): Mus musculus 
Inflammatory bowel diseases are highly debilitating conditions that require constant monitoring and life-long medication. Current treatments are focused on systemic administration of immunomodulatory drugs, but they have a broad range of undesirable side-effects. The RNA interference is a highly spe...
ORGANISM(S): Homo sapiens 
Background Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease with few treatment options, rendering the development of new, effective therapeutics of critical importance. The immune system plays a substantial role in ALS pathology, with multiple cell populations implicated in ...
ORGANISM(S): Mus musculus 
Here we elucidate the molecular mechanism of tofacitinib, an oral Janus kinase inhibitor, in psoriasis. Tofacitinib exhibits a multi-tiered action, with early direct effects on keratinocytes and histological and transcriptomic improvement prior to IL-17 reduction. Twelve patients with plaque psorias...
ORGANISM(S): Homo sapiens 
T Cell stretch-enhancers are vulnerable to Jak inhibitor tofacitinib Treatment of T cells with the Janus kinase (JAK) inhibitor, tofacitinib, disproportionately altered the expression of RA risk genes with stretech-enhancer (SE) structures.
ORGANISM(S): Homo sapiens 
Analysis of rectal transcriptome in ulcerative colitis (UC) patients who received tofacitinib
Effects of tofacitinib and takinib on autoimmune pancreatitis in mice
Evaluation of tofacitinib in cutaneous sarcoidosis [scRNA-seq]
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