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Source: The International Journal of Biochemistry and Cell Biology

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Total 120 results found since Jan 2013.

The AQP-3 water channel is a pivotal modulator of glycerol-induced chloride channel activation in nasopharyngeal carcinoma cells.
In conclusion, AQP-3 is the pathway for water, glycerol and other small solutes to enter cells, and it may be an essential modulator for the gating of chloride channels. PMID: 26794461 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - January 18, 2016 Category: Biochemistry Authors: Zhang H, Deng Z, Yang L, Luo H, Liu S, Li Y, Wei Y, Peng S, Zhu L, Wang L, Chen L Tags: Int J Biochem Cell Biol Source Type: research

Notch1 Inhibition Reduces Low Shear Stress-Induced Plaque Formation.
Abstract Low shear stress (LSS) contributes to the pathogenesis of inflammatory diseases, such as atherosclerosis. Notch1 is a type I transmembrane receptor that critically determines the growth, differentiation, and survival of various cell types, but its role and mechanism in LSS-induced inflammatory response remains undetermined. Apolipoprotein E-deficient (ApoE(-/-)) mice were fed with high fat diet and administered intraperitoneally with DAPT (a γ-secretase inhibitor). Perivascular shear stress modifiers were placed around the right carotid arteries to induce LSS. The left carotid arteries with undisturbed s...
Source: The International Journal of Biochemistry and Cell Biology - January 16, 2016 Category: Biochemistry Authors: Qin WD, Zhang F, Qin XJ, Wang J, Meng X, Wang H, Guo HP, Wu QZ, Wu DW, Zhang MX Tags: Int J Biochem Cell Biol Source Type: research

Cross-talk between EPAS-1/HIF-2α and PXR Signaling Pathway Regulates Multi-drug Resistance of Stomach Cancer Cell.
In this study, we found that EPAS-1 would promote the growth of stomach cancer cell line BGC-823. Our results revealed that EPAS-1 interacts with Pregnane X Receptor (PXR), a nuclear receptor that regulates multiple genes' transcription involved in multi-drugs resistance (MDR) process. Protein-protein interaction between EPAS-1 and PXR was identified by co-immunoprecipitation and GST-pull down assays. By this interaction, EPAS-1 recruited PXR to its response elements in promoter/enhancer regions of CYP3A4, a PXR target gene. Over-expression of EPAS-1 increased the expression of PXR responsive genes, enhanced the proliferat...
Source: The International Journal of Biochemistry and Cell Biology - January 16, 2016 Category: Biochemistry Authors: Zhao J, Bai Z, Feng F, Song E, Du F, Zhao J, Shen G, Ji F, Li G, Ma X, Hang X, Xu B Tags: Int J Biochem Cell Biol Source Type: research

Fibrillin-1 mgΔ(lpn) Marfan syndrome mutation associates with preserved proteostasis and bypass of a protein disulfide isomerase-dependent quality checkpoint.
Abstract Fibrillin-1 mutations promote Marfan syndrome (MFS) via complex yet unclear pathways. The roles of endoplasmic reticulum (ER) and the major ER redox chaperone protein disulfide isomerase-A1 in the processing of normal and mutated fibrillin-1 and ensuing protein secretion and/or intracellular retention are unclear. Our results in mouse embryonic fibroblasts bearing the exon-skipping mgΔ(lox-P-neo) (mgΔ(lpn)) mutation, which associates in vivo with MFS and in vitro with disrupted microfibrils, indicate a preserved ER-dependent proteostasis or redox homeostasis. Rather, mutated fibrillin-1 is secreted norm...
Source: The International Journal of Biochemistry and Cell Biology - December 21, 2015 Category: Biochemistry Authors: Meirelles T, Araujo TL, Nolasco P, Moretti AI, Guido MC, Debbas V, Pereira LV, Laurindo FR Tags: Int J Biochem Cell Biol Source Type: research

NLRC5 regulates TGF-β1-induced proliferation and activation of hepatic stellate cells during hepatic fibrosis.
Abstract Therapeutic management of liver fibrosis remains an unsolved clinical problem. Hepatic accumulation of extracellular matrix, mainly collagen, is mediated by the production of transforming growth factor-β1 (TGF-β1) in hepatic stellate cells (HSCs). NLRC5, the largest member of the NLR protein family, has recently been identified as a critical regulator of immune responses. Novel evidence shows that NLRC5 is an important negative modulator of inflammatory pathways. Herein, we determined the regulation of NLRC5 in liver fibrogenesis and its underlying mechanisms. We have shown that NLRC5 was upregulated in...
Source: The International Journal of Biochemistry and Cell Biology - November 16, 2015 Category: Biochemistry Authors: Xu T, Ni MM, Xing-Li, Li XF, Meng XM, Huang C, Li J Tags: Int J Biochem Cell Biol Source Type: research

APC functions at the centrosome to stimulate microtubule growth.
Abstract The adenomatous polyposis coli (APC) tumor suppressor is multi-functional. APC is known to localize at the centrosome, and in mitotic cells contributes to formation of the mitotic spindle. To test whether APC contributes to nascent microtubule (MT) growth at interphase centrosomes, we employed MT regrowth assays in U2OS cells to measure MT assembly before and after nocodazole treatment and release. We showed that siRNA knockdown of full-length APC delayed both initial MT aster formation and MT elongation/regrowth. In contrast, APC-mutant SW480 cancer cells displayed a defect in MT regrowth that was unaffe...
Source: The International Journal of Biochemistry and Cell Biology - November 7, 2015 Category: Biochemistry Authors: Lui C, Ashton C, Sharma M, Brocardo MG, Henderson BR Tags: Int J Biochem Cell Biol Source Type: research

Sodium butyrate down-regulates Tristetraprolin-mediated cyclin B1 expression independent of the formation of processing bodies.
Abstract Butyrate regulates multiple host cellular events including the cell cycle; however, little is known about the molecular mechanism by which butyrate induces a global down-regulation of the expression of genes associated with the cell cycle. Here, we demonstrate that treating HEK293T cells and the non-small-cell lung cancer cell line A549 with a high concentration of sodium butyrate reduces cyclin B1 expression. The underlying mechanism is related to the destabilization of its mRNA by tristetraprolin, which is up-regulated in response to sodium butyrate. Specifically, the sodium butyrate stimulation reduces...
Source: The International Journal of Biochemistry and Cell Biology - November 6, 2015 Category: Biochemistry Authors: Zheng XT, Xiao XQ Tags: Int J Biochem Cell Biol Source Type: research

TLR2-MyD88-NF-κB pathway is involved in tubulointerstitial inflammation caused by proteinuria.
In this study, we hypothesized whether the activation of the TLR2-MyD88-NF-κB pathway is involved in tubulointerstitial inflammation induced by proteinuria. We observed expression of TLR2, MyD88, NF-κB, as well as TNF-α and IL-6 detected by immunohistostaining, Western blotting and real-time PCR in albumin-overloaded (AO) nephropathy rats. In vitro, we observed these markers in HK-2 cells stimulated by albumin. We used TLR2 siRNA or the NF-κB inhibitor BAY 11-7082 to observe the influence of TNF-α and IL-6 expression caused by albumin overload. Finally, we studied these markers in non-IgA mesangioproliferative glomeru...
Source: The International Journal of Biochemistry and Cell Biology - October 17, 2015 Category: Biochemistry Authors: Ding LH, Liu D, Xu M, Wu M, Liu H, Tang RN, Ma KL, Chen PS, Liu BC Tags: Int J Biochem Cell Biol Source Type: research

Voltage-gated calcium channel blockers deregulate macroautophagy in cardiomyocytes.
VOLTAGE-GATED CALCIUM CHANNEL BLOCKERS DEREGULATE MACROAUTOPHAGY IN CARDIOMYOCYTES. Int J Biochem Cell Biol. 2015 Sep 28; Authors: Pushparaj C, Das A, Purroy R, Nàger M, Herreros J, Pamplona R, Cantí C Abstract Voltage-gated calcium channel blockers are widely used for the management of cardiovascular diseases, however little is known about their effects on cardiac cells in vitro. We challenged neonatal ventricular cardiomyocytes (CMs) with therapeutic L-type and T-type Ca(2+) channel blockers (nifedipine and mibefradil, respectively), and measured their effects on cell stress and survival, using fl...
Source: The International Journal of Biochemistry and Cell Biology - September 28, 2015 Category: Biochemistry Authors: Pushparaj C, Das A, Purroy R, Nàger M, Herreros J, Pamplona R, Cantí C Tags: Int J Biochem Cell Biol Source Type: research

Endoplasmic reticulum stress mediates the arsenic trioxide-induced apoptosis in human hepatocellular carcinoma cells.
Abstract Arsenic trioxide has been proven to trigger apoptosis in human hepatocellular carcinoma cells. And endoplasmic reticulum stress has been known to be involved in apoptosis through the induction of CCAAT/enhancer-binding protein homologous protein. However, it is unknown whether endoplasmic reticulum stress mediates arsenic trioxide-induced apoptosis in human hepatocellular carcinoma cells. Our data showed that arsenic trioxide significantly induced apoptosis in human hepatocellular carcinoma cells. Furthermore, arsenic trioxide triggered endoplasmic reticulum stress, as indicated by endoplasmic reticulum d...
Source: The International Journal of Biochemistry and Cell Biology - September 24, 2015 Category: Biochemistry Authors: Zhang XY, Yang SM, Zhang HP, Yang Y, Sun SB, Chang JP, Tao XC, Yang TY, Liu C, Yang YM Tags: Int J Biochem Cell Biol Source Type: research

AKT mediated glycolytic shift regulates autophagy in classically activated macrophages.
Abstract Autophagy is considered as an innate defense mechanism primarily due to its role in the targeting of intracellular pathogens for lysosomal degradation. Here we report inhibition of autophagy as an adaptive response in classically activated macrophages that helps achieve high cellular ROS production and cell death-another hallmark of innate mechanisms. We show prolonged classical activation of Raw 264.7 macrophages by treating them with IFN-γ and LPS inhibited autophagy. The inhibition of autophagy was dependent on nitric oxide (NO) production which activated the AKT-mTOR signaling, the known negative reg...
Source: The International Journal of Biochemistry and Cell Biology - July 26, 2015 Category: Biochemistry Authors: Matta SK, Kumar D Tags: Int J Biochem Cell Biol Source Type: research

The role of epigenetics in the endothelial cell shear stress response and atherosclerosis.
This article is part of a Directed Issue entitled: Epigenetics dynamics in development and disease. PMID: 25979369 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - May 13, 2015 Category: Biochemistry Authors: Dunn J, Simmons R, Thabet S, Jo H Tags: Int J Biochem Cell Biol Source Type: research

Amyloid-beta mediates the receptor of advanced glycation end product-induced pro-inflammatory response via toll-like receptor 4 signaling pathway in retinal ganglion cell line RGC-5.
Abstract Patients with diabetes mellitus have an increased risk of developing Alzheimer's disease. Amyloid-β, a product of amyloid precursor protein, is associated with neuro-inflammation in patients with Alzheimer's diseases. The correlation between amyloid-beta and advanced glycation end products, which accumulate in tissue of diabetic patients, is not clear. The aims of this study were to determine the effect of advanced glycation end product on the expression of amyloid precursor protein/amyloid-beta and associated pro-inflammatory responses in retinal ganglion cell line RGC-5. Treatment with advanced glycati...
Source: The International Journal of Biochemistry and Cell Biology - March 14, 2015 Category: Biochemistry Authors: Lee JJ, Wang PW, Yang IH, Wu CL, Chuang JH Tags: Int J Biochem Cell Biol Source Type: research

PPARδ modulates oxLDL-induced apoptosis of vascular smooth muscle cells through a TGF-β/FAK signaling axis.
Abstract The peroxisome proliferator-activated receptor delta (PPARδ) has been implicated in the modulation of vascular homeostasis. However, its roles in the apoptotic cell death of vascular smooth muscle cells (VSMCs) are poorly understood. Here, we demonstrate that PPARδ modulates oxidized low-density lipoprotein (oxLDL)-induced apoptosis of VSMCs through the transforming growth factor-β (TGF-β) and focal adhesion kinase (FAK) signaling pathways. Activation of PPARδ by GW501516, which is a specific ligand, significantly inhibited oxLDL-induced cell death and generation of reactive oxygen species in VSMCs. ...
Source: The International Journal of Biochemistry and Cell Biology - February 27, 2015 Category: Biochemistry Authors: Hwang JS, Eun SY, Ham SA, Yoo T, Lee WJ, Paek KS, Do JT, Lim DS, Seo HG Tags: Int J Biochem Cell Biol Source Type: research

Ataxia telangiectasia mutated inhibits oxidative stress-induced apoptosis by regulating heme oxygenase-1 expression.
In conclusion, ATM induces HO-1 expression via activation of PKC-δ and NF-κB and inhibits oxidative stress-induced apoptosis. A loss of HO-1 induction may explain why AT patients are vulnerable to oxidative stress. PMID: 25592228 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - January 12, 2015 Category: Biochemistry Authors: Yu JH, Cho SO, Lim JW, Kim N, Kim H Tags: Int J Biochem Cell Biol Source Type: research