K3.1 regulates cell cycle progression by modulating Ca signaling in murine preosteoblasts.

Osteoblasts synthesize and deposit essential components of the extracellular bone matrix and collagen scaffolds, leading to mineralized bone formation. Therefore, the proliferation of preosteoblasts (precursors of mature osteoblasts) helps in regulating skeletal homeostasis. This study demonstrated that the functional expression of K3.

Downregulation of IL-8 and IL-10 by the Activation of Ca-Activated K Channel K3.1 in THP-1-Derived M Macrophages.

THP-1-differentiated macrophages are useful for investigating the physiological significance of tumor-associated macrophages (TAMs). In the tumor microenvironment (TME), TAMs with the M-like phenotype play a critical role in promoting cancer progression and metastasis by inhibiting the immune surveillance system. We examined the involvement of Ca-activated K channel K3.

K1.1 K Channel Inhibition Overcomes Resistance to Antiandrogens and Doxorubicin in a Human Prostate Cancer LNCaP Spheroid Model.

Several types of K channels play crucial roles in tumorigenicity, stemness, invasiveness, and drug resistance in cancer. Spheroid formation of human prostate cancer (PC) LNCaP cells with ultra-low attachment surface cultureware induced the up-regulation of cancer stem cell markers, such as NANOG, and decreased the protein degradation of the Ca-activated K channel K1.1 by down-regulating the E3 ubiquitin ligase, FBXW7, compared with LNCaP monolayers.

K3.1 inhibition-induced activation of the JNK/c-Jun signaling pathway enhances IL-10 expression in peripherally-induced regulatory T cells.

The K3.1 inhibition up-regulates IL-10 expression in regulatory T (T) cells in the recovery phase of inflammatory bowel disease (IBD) model mice; however, the underlying signaling pathway remains unclear. We investigated the involvement of AP-1 (Fos/Jun) and NF-κB in the expression of IL-10 and its transcription factors (TFs) in in vitro-induced mouse splenic T cells.

Ca -activated K channel K 1.1 as a therapeutic target to overcome chemoresistance in three-dimensional sarcoma spheroid models.

The large-conductance Ca -activated K channel K 1.1 plays a pivotal role in tumor development and progression in several solid cancers. The three-dimensional (3D) in vitro cell culture system is a powerful tool for cancer spheroid formation, and mimics in vivo solid tumor resistance to chemotherapy in the tumor microenvironment (TME).

Downregulation of the Ca-activated K channel K3.1 in mouse preosteoblast cells treated with vitamin D receptor agonist.

The maturity of osteoblasts by proliferation and differentiation in preosteoblasts is essential for maintaining bone homeostasis. The beneficial effects of vitamin D on bone homeostasis in mammals have been demonstrated experimentally and clinically. However, the direct actions of vitamin D on preosteoblasts remain to be fully elucidated.

Possible Contribution of Inflammation-Associated Hypoxia to Increased K5.1 K Channel Expression in CD4 T cells of the Mouse Model for Inflammatory Bowel Disease.

Previous studies have reported the up-regulation of the two-pore domain K channel K5.1 in the CD4 T cells of patients with multiple sclerosis (MS) and rheumatoid arthritis (RA), as well as in a mouse model of inflammatory bowel disease (IBD). However, the mechanisms underlying this up-regulation remain unclear.

Inhibition of Interleukin 10 Transcription through the SMAD2/3 Signaling Pathway by Ca-Activated K Channel K3.1 Activation in Human T-Cell Lymphoma HuT-78 Cells.

The hyperpolarization induced by intermediate-conductance Ca-activated K channel (K3.1) activation increases the driving force for Ca influx, which generally promotes cell proliferation, migration, and cytokine production in immunocompetent cells. Interleukin-10 (IL-10) from tumor-infiltrating lymphocytes and macrophages, lymphoma, and carcinoma cells facilitates escape from cancer immune surveillance; however, the role of K3.

Histone Deacetylases Enhance Ca-Activated K⁺ Channel K3.1 Expression in Murine Inflammatory CD4⁺ T Cells.

The up-regulated expression of the Ca-activated K⁺ channel K3.1 in inflammatory CD4⁺ T cells has been implicated in the pathogenesis of inflammatory bowel disease (IBD) through the enhanced production of inflammatory cytokines, such as interferon-γ (IFN-γ). However, the underlying mechanisms have not yet been elucidated.

Defective splicing of the background K channel K5.1 by the pre-mRNA splicing inhibitor, pladienolide B in lectin-activated mouse splenic CD4 T cells.

The two-pore domain K channel K5.1 has been implicated in the pathogenesis of autoimmune diseases. We investigated the changes in K5.

Pathophysiological significance of the two-pore domain K(+) channel K2P5.1 in splenic CD4(+)CD25(-) T cell subset from a chemically-induced murine inflammatory bowel disease model.

The alkaline pH-activated, two-pore domain K(+) channel K2P5.1 (also known as TASK2/KCNK5) plays an important role in maintaining the resting membrane potential, and contributes to the control of Ca(2+) signaling in several types of cells. Recent studies highlighted the potential role of the K2P5.

Molecular identification of the dominant-negative, splicing isoform of the two-pore domain K(+) channel K(2P)5.1 in lymphoid cells and enhancement of its expression by splicing inhibition.

The two-pore domain background K(+) channel K2P5.1 is expected as a possible therapeutic target for autoimmune and inflammatory disorders and cancers because it plays an important role in maintaining the resting membrane potential and regulation of Ca(2+) signaling in T lymphocytes and cancer cells. However, the lack of selective K2P5.

Host specificity and in vivo infectivities of the mouse coccidian parasites Eimeria krijgsmanni.

In the present study, infection experiments of E. krijgsmanni using various hosts were conducted to elucidate the host specificity among some animals and the infectivity to mouse strains. According to the results, the infection was not found in most animals, except for rats, in which some oocyst shedding was detected, and there was no significant difference in infectivity among mouse strains.

Genetic changes of coxsackievirus A16 and enterovirus 71 isolated from hand, foot, and mouth disease patients in Toyama, Japan between 1981 and 2007.

We characterized the genetic diversity of the complete VP1 region of coxsackievirus A16 (CA16) and enterovirus 71 (EV71) isolated from patients with hand, foot, and mouth disease in Toyama from 1981 to 2007 to evaluate the relationship between epidemics and genetic changes. The predominant genogroups of CA16 changed from B to C in 1995-1998, and genogroup C further changed from subgenogroup C1 to C2 around 2002, and to C3 in 2005-2007. The subgenogroups of the EV71 isolates were classified into B1, B4, C1, and C3 in 1983-1994, and into C4 in 1997-2006.