ArticlePloS one2012
Homeodomain-interacting protein kinase (HIPK)-1 is required for splenic B cell homeostasis and optimal T-independent type 2 humoral response.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Identification of ROCK1 as a novel biomarker for postmenopausal osteoporosis and pan-cancer analysis.Aging · 2023Article
- Identification of HIPK3 as a potential biomarker and an inhibitor of clear cell renal cell carcinoma.Aging · 2021Article
- Mapping effector genes at lupus GWAS loci using promoter Capture-C in follicular helper T cells.Nature communications · 2020Article
- HIPK3 Mediates Inflammatory Cytokines and Oxidative Stress Markers in Monocytes in a Rat Model of Sepsis Through the JNK/c-Jun Signaling Pathway.Inflammation · 2020Article
- Coordinated signals from the DNA repair enzymes PARP-1 and PARP-2 promotes B-cell development and function.Cell death and differentiation · 2019Article
- Cell extrinsic alterations in splenic B cell maturation in Flt3-ligand knockout mice.Immunity, inflammation and disease · 2015Article
- Phosphorylation of Krüppel-like factor 3 (KLF3/BKLF) and C-terminal binding protein 2 (CtBP2) by homeodomain-interacting protein kinase 2 (HIPK2) modulates KLF3 DNA binding and activity.The Journal of biological chemistry · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The homeodomain-interacting protein kinase (HIPK) family is comprised of four highly related serine/threonine kinases originally identified as co-repressors for various homeodomain-containing transcription factors. The HIPKs have been shown to be involved in growth regulation and apoptosis, with numerous studies highlighting HIPK regulation of the tumor suppressor p53. In this study, we have discovered a B cell homeostatic defect in HIPK1-deficient (HIPK1(-/-)) mice. Lymphopoietic populations within the thymus and bone marrow of HIPK1(-/-) mice appeared normal based upon FACS analysis; however, the spleen exhibited a reduced number of total B cells with a significant loss of transitional-1 and follicular B cell populations. Interestingly, the marginal zone B cell population was expanded in HIPK1(-/-) mice, yielding an increased frequency of these cells. HIPK1(-/-) B cells exhibited impaired cell division in response to B cell receptor cross-linking in vitro based upon thymidine incorporation or CFSE dilution; however, the addition of CD40L rescued HIPK1(-/-) proliferation to wild-type levels. Despite the expanded MZ B cell population in the HIPK1(-/-) mice, the T-independent type 2 humoral response was impaired. These data identify HIPK1 as a novel kinase required for optimal B cell function in mice.
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