ArticleMolecular cancer research : MCR2017
Nuclear Import of JAK1 Is Mediated by a Classical NLS and Is Required for Survival of Diffuse Large B-cell Lymphoma.
Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- FERM domain-containing proteins are active components of the cell nucleus.Life science alliance · 2024Review
- Double-edged sword of JAK/STAT signaling pathway in viral infections: novel insights into virotherapy.Cell communication and signaling : CCS · 2023Review
- EGR1 Addiction in Diffuse Large B-cell Lymphoma.Molecular cancer research : MCR · 2021Article
- JAK3 Is Expressed in the Nucleus of Malignant T Cells in Cutaneous T Cell Lymphoma (CTCL).Cancers · 2021Article
- The Seminiferous Epithelial Cycle of Spermatogenesis: Role of Non-receptor Tyrosine Kinases.Advances in experimental medicine and biology · 2021Article
- Identification of a 14-Gene Prognostic Signature for Diffuse Large B Cell Lymphoma (DLBCL).Frontiers in genetics · 2021Article
- Review
- STAT3 Activation and Oncogenesis in Lymphoma.Cancers · 2019Review
- Janus Kinase 1 Is Required for Transcriptional Reprograming of Murine Astrocytes in Response to Endoplasmic Reticulum Stress.Frontiers in cellular neuroscience · 2019Article
- Gene regulation and suppression of type I interferon signaling by STAT3 in diffuse large B cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Glutaminolysis Mediated by MALT1 Protease Activity Facilitates PD-L1 Expression on ABC-DLBCL Cells and Contributes to Their Immune Evasion.Frontiers in oncology · 2018Article
- HiJAKing the epigenome in leukemia and lymphoma.Leukemia & lymphoma · 2017Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
JAKs are non-receptor tyrosine kinases that are generally found in association with cytokine receptors. In the canonical pathway, roles of JAKs have well been established in activating STATs in response to cytokine stimulation to modulate gene transcription. In contrast, a noncanonical role of JAK2 has recently been discovered, in which JAK2 in the nucleus imparts the epigenetic regulation of gene transcription through phosphorylation of tyrosine 41 on the histone protein H3. Recent work further demonstrated that this noncanonical mechanism is conserved with JAK1, which is activated by the autocrine cytokines IL6 and IL10 in activated B-cell-like diffuse large B-cell lymphoma (ABC DLBCL), a cancer type that is particularly difficult to treat and has poor prognosis. However, how JAK1 gains access to the nucleus to enable epigenetic regulation remains undefined. Here, we investigated this question and revealed that JAK1 has a classical nuclear localization signal toward the N-terminal region, which can be recognized by multiple importin α isoforms. Moreover, the nuclear import of JAK1 is independent of its kinase activity but is required for the optimal expansion of ABC DLBCL cells
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