Tyrosine kinase c-Abl regulates the survival of plasma cells

Li, Yanfeng; Xu, Shengli; Huang, Yuhan; Ou, Xijun; Lam, Kong-Peng

doi:10.1038/srep40133

Cited by 6 publications

(6 citation statements)

References 42 publications

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“…a new transcriptional cell program). Finally, overexpression of ABL1 confirms previous observations by Li et al ( 43 ) which revealed the role of this tyrosine kinase on PC survival.…”

Section: Discussionsupporting

confidence: 90%

Dynamic Intracellular Metabolic Cell Signaling Profiles During Ag-Dependent B-Cell Differentiation

et al. 2021

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Human B-cell differentiation has been extensively investigated on genomic and transcriptomic grounds; however, no studies have accomplished so far detailed analysis of antigen-dependent maturation-associated human B-cell populations from a proteomic perspective. Here, we investigate for the first time the quantitative proteomic profiles of B-cells undergoing antigen-dependent maturation using a label-free LC-MS/MS approach applied on 5 purified B-cell subpopulations (naive, centroblasts, centrocytes, memory and plasma B-cells) from human tonsils (data are available via ProteomeXchange with identifier PXD006191). Our results revealed that the actual differences among these B-cell subpopulations are a combination of expression of a few maturation stage-specific proteins within each B-cell subset and maturation-associated changes in relative protein expression levels, which are related with metabolic regulation. The considerable overlap of the proteome of the 5 studied B-cell subsets strengthens the key role of the regulation of the stoichiometry of molecules associated with metabolic regulation and programming, among other signaling cascades (such as antigen recognition and presentation and cell survival) crucial for the transition between each B-cell maturation stage.

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“…a new transcriptional cell program). Finally, overexpression of ABL1 confirms previous observations by Li et al ( 43 ) which revealed the role of this tyrosine kinase on PC survival.…”

Section: Discussionsupporting

confidence: 90%

Dynamic Intracellular Metabolic Cell Signaling Profiles During Ag-Dependent B-Cell Differentiation

et al. 2021

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“…In our previous work, we summarized that ROS may regulate the expression of ABL1 by triggering receptor tyrosine kinases (RTKs), which subsequently led to the phosphorylation of ABL1. NF- κ B1 and STAT3 were the main factors involved in cytokine release [29, 30], and both NF- κ B1 and STAT3 were proven to be downstream targets of ABL1 in leukemia [31, 32]. Here, we treated SGC-7901 and AGS GC cell lines with different concentrations of H 2 O 2 (0 μ M, 25 μ M, and 50 μ M), and the result showed that ROS could enhance the activities of ABL1 and could upregulate p-NF- κ B1, p-STAT3, IL-6, IL-1 β , and COX2 (Figure 2(a)).…”

Section: Resultsmentioning

confidence: 99%

“…NF- κ B1 and STAT3 are crucial factors regulating the tumor microenvironment. Both NF- κ B and STAT3 are proven to be downstream targets of ABL1 in leukemia [31, 32]. The constitutive activation of NF- κ B1 leads to cytokine release (TNF α , IL-6, IL-1, and IL-8), and these cytokines can give a positive feedback loop to induce the activation of NF- κ B [38–40].…”

Section: Discussionmentioning

confidence: 99%

Reactive Oxygen Species Are Involved in the Development of Gastric Cancer and Gastric Cancer-Related Depression through ABL1-Mediated Inflammation Signaling Pathway

Huang

Zhou

Yuan

et al. 2019

Oxidative Medicine and Cellular Longevity

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Background. The mechanisms of crosstalk between depression and gastric cancer (GC) remain ill defined. Given that reactive oxygen species (ROS) is involved in the pathophysiology of both GC and depression, we try to explore the activities of ROS in the development of GC and GC-related depression. Methods. 110 patients with newly diagnosed GC were recruited in our study. The clinical characteristics of these patients were recorded. Inflammation and oxidative stress markers were detected by ELISA. The depression status of patients with GC was assessed during follow-up. The association between ROS, ABL1, and inflammation factors was evaluated in H2O2-treated GC cell lines and The Cancer Genome Atlas (TCGA) database. The effect of ABL1 on inflammation was detected with Imatinib/Nilotinib-treated GC cell lines. A chronic mild stress- (CMS-) induced patient-derived xenograft (PDX) mice model was established to assess the crosstalk between depression and GC. Results. Depression was correlated with poor prognosis of patients with GC. GC patients with depression were under a high level of oxidative status as well as dysregulated inflammation. In the CMS-induced GC PDX mice model, CMS could facilitate the development of GC. Additionally, tumor bearing could induce depressive-like behaviors of mice. With the treatment of ROS, the activities of ABL1 and inflammatory signaling were enhanced both in vitro and in vivo, and blocking the activities of ABL1 inhibited inflammatory signaling. Conclusions. ROS-activated ABL1 mediates inflammation through regulating NF-κB1 and STAT3, which subsequently leads to the development of GC and GC-related depression.

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“…For example, T cells in Bim-deficient mice are defective in TCR-induced activation and IL-2 production due to impaired calcium signaling (72). Additionally, T cell development is impaired at the DN to DP stages in the thymus altering T cellular composition and repertoire in the Bim-deficient mice (73). Alternatively, global loss of Bim in the whole body reduces release of self-antigens from dead and dying host cells that trigger autoimmune response.…”

Section: Discussionmentioning

confidence: 99%

Impaired B Cell Apoptosis Results in Autoimmunity That Is Alleviated by Ablation of Btk

et al. 2021

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While apoptosis plays a role in B-cell self-tolerance, its significance in preventing autoimmunity remains unclear. Here, we report that dysregulated B cell apoptosis leads to delayed onset autoimmune phenotype in mice. Our longitudinal studies revealed that mice with B cell-specific deletion of pro-apoptotic Bim (BBimfl/fl) have an expanded B cell compartment with a notable increase in transitional, antibody secreting and recently described double negative (DN) B cells. They develop greater hypergammaglobulinemia than mice lacking Bim in all cells and accumulate several autoantibodies characteristic of Systemic Lupus Erythematosus (SLE) and related Sjögren’s Syndrome (SS) including anti-nuclear, anti-Ro/SSA and anti-La/SSB at a level comparable to NODH2h4 autoimmune mouse model. Furthermore, lymphocytes infiltrated the tissues including submandibular glands and formed follicle-like structures populated with B cells, plasma cells and T follicular helper cells indicative of ongoing immune reaction. This autoimmunity was ameliorated upon deletion of Bruton’s tyrosine kinase (Btk) gene, which encodes a key B cell signaling protein. These studies suggest that Bim-mediated apoptosis suppresses and B cell tyrosine kinase signaling promotes B cell-mediated autoimmunity.

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Tyrosine kinase c-Abl regulates the survival of plasma cells

Cited by 6 publications

References 42 publications

Dynamic Intracellular Metabolic Cell Signaling Profiles During Ag-Dependent B-Cell Differentiation

Dynamic Intracellular Metabolic Cell Signaling Profiles During Ag-Dependent B-Cell Differentiation

Reactive Oxygen Species Are Involved in the Development of Gastric Cancer and Gastric Cancer-Related Depression through ABL1-Mediated Inflammation Signaling Pathway

Impaired B Cell Apoptosis Results in Autoimmunity That Is Alleviated by Ablation of Btk

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