Involvement of cell cycle progression in survival signaling through CD40 in the B-lymphocyte line WEHI-231

Hirai, Hiroyuki; Adachi, Takahiro; Tsubata, Takeshi

doi:10.1038/sj.cdd.4401357

Cited by 14 publications

(8 citation statements)

References 50 publications

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“…In fact, the interaction between CD40 on B cells and CD40L on activated T cells has several additional effects. It not only leads to B cell activation, differentiation, proliferation and antibody production, but it also up-regulates the expression of the anti-apoptotic molecule Bcl-2 [98][99][100]. The latter effect may allow prolactin to rescue autoreactive B cells from negative selection and, thereby, fosters breakdown of tolerance to self [73].…”

Section: Prolactin and The Humoral Responsementioning

confidence: 95%

Spotlight on the role of hormonal factors in the emergence of autoreactive B-lymphocytes

2005

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Section: Prolactin and The Humoral Responsementioning

confidence: 95%

Spotlight on the role of hormonal factors in the emergence of autoreactive B-lymphocytes

2005

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“…Stimulation of B cells through CD40 results in the induction of G1/S cyclin-D2 and degradation of cyclin inhibitor p27 kip-1 , which are critical for cell-cycle progression [38,44,45]. As CD40-induced proliferation is defective in CARMA1 KO B cells, we sought to determine the induction of cyclin-D2 and degradation of p27 kip-1 upon CD40 stimulation.…”

Section: Cell-cycle Progression In Cd40-stimulated Carma1 Ko B Cellsmentioning

confidence: 99%

Potential role of CARMA1 in CD40‐induced splenic B cell proliferation and marginal zone B cell maturation

Pappu¹,

Lin²

2006

Eur J Immunol

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NF‐κB activation through B cell receptor (BCR) ligation is critical for B cell development, survival and antigen‐mediated activation of B cells. CARD domain and MAGUK‐domain containing protein‐1 (CARMA1), recently identified adaptor molecule, has been shown to play an essential role in BCR‐induced NF‐κB activation. CARMA1‐deficient B cells fail to proliferate upon BCR stimulation, leading to defective humoral responses. Surprisingly, CARMA1‐deficient B cells are also defective in CD40‐induced proliferation. The mechanisms responsible for CD40‐induced proliferation defect have not yet been characterized. In this study, we show that signaling cascades activated by CD40 stimulation are largely unaffected in CARMA1‐deficient B cells. Instead, we have found that the defective proliferation of CARMA1‐deficient B cells is due to two events. First, CARMA1‐deficient B cells show defective cell‐cycle progression. Secondly, the numbers of marginal zone (MZ) B cells, which are the main responders upon CD40 stimulation, are greatly diminished in CARMA1‐deficient mice. Since B cell maturation requires basal signaling through BCR and NF‐κB activation, we propose that impaired BCR signaling in CARMA1‐deficient mice leads to defective maturation of MZ B cell population, which in turn, contributes to impaired proliferation upon CD40 stimulation.

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“…GI carcinoid cells treated with or without VPA were labeled for 1 hour with 10 M bromodeoxyuridine (Sigma-Aldrich), counterstained with 50 g/ml propidium iodide, and analyzed by two-dimensional flow cytometry (FACSCalibur flow cytometer; BD Biosciences) to detect both fluorescein and propidium iodide as previously described [13]. Results were analyzed with FlowJo software (Tree Star, Ashland, OR).…”

Section: Flow Cytometrymentioning

confidence: 99%

Valproic Acid Activates Notch-1 Signaling and Regulates the Neuroendocrine Phenotype in Carcinoid Cancer Cells

et al. 2007

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Carcinoid tumors are neuroendocrine malignancies that frequently metastasize and secrete hormones that cause debilitating symptoms in patients. In this study we report the effects of valproic acid (VPA), a drug long used for the treatment of epilepsy, on the growth and neuroendocrine phenotype of human carcinoid cancer cells. VPA treatment of gastrointestinal and pulmonary carcinoid cells resulted in a dose-dependent inhibition of cancer cell growth. Western blot analysis revealed degradation of cyclin D1 and an increase in cyclin-dependent kinases p21 and p27 with VPA treatment. Flow cytometry confirmed that the mechanism of VPA-induced growth inhibition is G 1 phase cell cycle arrest. Furthermore, VPA suppressed expression of the neuroendocrine tumor marker chromogranin A. In addition to these effects, VPA also increased levels of full- Disclosure of potential conflicts of interest is found at the end of this article.

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Involvement of cell cycle progression in survival signaling through CD40 in the B-lymphocyte line WEHI-231

Cited by 14 publications

References 50 publications

Spotlight on the role of hormonal factors in the emergence of autoreactive B-lymphocytes

Spotlight on the role of hormonal factors in the emergence of autoreactive B-lymphocytes

Potential role of CARMA1 in CD40‐induced splenic B cell proliferation and marginal zone B cell maturation

Valproic Acid Activates Notch-1 Signaling and Regulates the Neuroendocrine Phenotype in Carcinoid Cancer Cells

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