Bibliografías temáticas / Hd62.4 .p38 2007

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Literatura académica sobre el tema "Hd62.4 .p38 2007"

Autor: Grafiati

Publicado: 27 de julio de 2024

Última modificación: 31 de julio de 2025

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Artículos de revistas sobre el tema "Hd62.4 .p38 2007"

Haisenleder, D. J., L. L. Burger, H. E. Walsh, et al. "Pulsatile Gonadotropin-Releasing Hormone Stimulation of Gonadotropin Subunit Transcription in Rat Pituitaries: Evidence for the Involvement of Jun N-Terminal Kinase But Not p38." Endocrinology 149, no. 1 (2007): 139–45. http://dx.doi.org/10.1210/en.2007-1113.

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We investigated whether Jun N-terminal kinase (JNK) and p38 mediate gonadotropin subunit transcriptional responses to pulsatile GnRH in normal rat pituitaries. A single pulse of GnRH or vehicle was given to female rats in vivo, pituitaries collected, and phosphorylated JNK and p38 measured. GnRH stimulated an increase in JNK phosphorylation within 5 min, which peaked 15 min after GnRH (3-fold). GnRH also increased p38 phosphorylation 2.3-fold 15 min after stimulus. Rat pituitary cells were given 60-min pulses of GnRH or media plus the JNK inhibitor SP600125 (SP, 20 μm), p38 inhibitor SB203580

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Hou, Ni, Seiji Torii, Naoya Saito, Masahiro Hosaka та Toshiyuki Takeuchi. "Reactive Oxygen Species-Mediated Pancreatic β-Cell Death Is Regulated by Interactions between Stress-Activated Protein Kinases, p38 and c-Jun N-Terminal Kinase, and Mitogen-Activated Protein Kinase Phosphatases". Endocrinology 149, № 4 (2008): 1654–65. http://dx.doi.org/10.1210/en.2007-0988.

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Pancreatic β-cells are susceptible to reactive oxygen species (ROS), which are known to be generated by high or low glucose (LG), hypoxic, or cytokine-producing conditions. When we cultured mouse β-cell-derived MIN6 cells in a LG condition, we detected a significant generation of ROS, including hydrogen peroxide, which was comparable to the ROS production in hypoxic or cytokine-treated conditions. ROS accumulation induced by the LG culture led to cell death, which was prevented by the ROS scavengers N-acetylcysteine and manganese(III)tetrakis(4-benzoic acid) porphyrin. We next investigated the

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Osorio, Juan C., Faisal H. Cheema, Timothy P. Martens, et al. "Simvastatin reverses cardiac hypertrophy caused by disruption of the bradykinin 2 receptorPresented in part at the American College of Cardiology meeting March 2003 in Orlando, USA, and the Society for Pediatric Research meeting May 2007 in Toronto, Canada." Canadian Journal of Physiology and Pharmacology 86, no. 9 (2008): 633–42. http://dx.doi.org/10.1139/y08-068.

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Bradykinin 2 receptor (B2R) deficiency predisposes to cardiac hypertrophy and hypertension. The pathways mediating these effects are not known. Two-month-old B2R knockout (KO) and wild-type (WT) mice were assigned to 4 treatment groups (n = 12–14/group): control (vehicle); nitro-l-arginine methyl ester (l-NAME) an NO synthase inhibitor; simvastatin (SIM), an NO synthase activator; and SIM+l-NAME. Serial echocardiography was performed and blood pressure (BP) at 6 weeks was recorded using a micromanometer. Myocardial eNOS and mitogen-activated protein kinase (MAPK, including ERK, p38, and JNK) p

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Ramanjaneya, Manjunath, Alex C. Conner, Jing Chen, Peter R. Stanfield, and Harpal S. Randeva. "Orexins Stimulate Steroidogenic Acute Regulatory Protein Expression through Multiple Signaling Pathways in Human Adrenal H295R Cells." Endocrinology 149, no. 8 (2008): 4106–15. http://dx.doi.org/10.1210/en.2007-1739.

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Orexins mediate a variety of physiological processes, including feeding behavior, the circadian pathway, and cortisol secretion. Steroidogenesis is regulated by a variety of neuropeptides, and one of the key rate-limiting steps is cholesterol transport across the mitochondrial membrane by the steroidogenic acute regulatory protein (StAR). StAR expression can be regulated through several different signaling pathways. Despite the clear link between orexins and steroid production, the actions of the orexin family of hormones on steroid biosynthesis are not fully understood. We present data showin

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Maraver, Antonio, Carlos E. Tadokoro, Michelle L. Badura, Jie Shen, Manuel Serrano, and Juan J. Lafaille. "Effect of presenilins in the apoptosis of thymocytes and homeostasis of CD8+ T cells." Blood 110, no. 9 (2007): 3218–25. http://dx.doi.org/10.1182/blood-2007-01-070359.

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Abstract Many studies have positioned Notch signaling at various critical junctions during T-cell development. There is, however, debate regarding the role of Notch in the CD4 versus CD8 lineage commitment. Because there are 4 Notch receptors and RBP-Jκ–independent Notch signaling has been reported, we decided to eliminate γ-secretase activity once its activity is required for all forms of Notch signaling. T-cell–specific elimination of γ-secretase was carried out by crossing presenilin-1 (PS1) floxed mice with CD4-Cre mice and PS2 KO mice, generating PS KO mice. Thymic CD4+CD8+ double-positiv

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Haugen, Fred, та Christian A. Drevon. "Activation of Nuclear Factor-κB by High Molecular Weight and Globular Adiponectin". Endocrinology 148, № 11 (2007): 5478–86. http://dx.doi.org/10.1210/en.2007-0370.

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Adipose tissue secretes a wide range of hormones named adipokines, and these may play a role in obesity-related inflammation. Adiponectin is an exceptional adipokine because low plasma concentrations are associated with obesity, type 2 diabetes, and cardiovascular diseases. It has been observed that plasma adiponectin concentrations are elevated during inflammatory conditions like preeclampsia and arthritis. Nuclear factor-κB (NF-κB) is an essential transcription factor for expression of inflammation-related proteins. We have used U937 cells stably transfected to express luciferase under the c

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Shankar, Kartik, Xiaoli Liu, Rohit Singhal, et al. "Chronic Ethanol Consumption Leads to Disruption of Vitamin D3 Homeostasis Associated with Induction of Renal 1,25 Dihydroxyvitamin D3-24-Hydroxylase (CYP24A1)." Endocrinology 149, no. 4 (2007): 1748–56. http://dx.doi.org/10.1210/en.2007-0903.

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Bone loss resulting from chronic ethanol (EtOH) abuse is frequently accompanied by altered vitamin D3 homeostasis. In the current study, we examined EtOH effects in a female rat model in which control or EtOH-containing diets were infused intragastrically. EtOH treatment reduced plasma 1,25-dihydroxycholecalciferol (1,25 (OH)2 D3) coincident with a decrease in renal CYP27B1 (25(OH)D3 1α-hydroxylase) mRNA and an increase in expression of renal CYP24A1 (1,25 (OH)2 D3- 24-hydroxylase). EtOH induction of CYP24A1 occurred as a result of increased transcription and was also observed in vitro in prim

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Csóka, Balázs, Zoltán H. Németh, László Virág та ін. "A2A adenosine receptors and C/EBPβ are crucially required for IL-10 production by macrophages exposed to Escherichia coli". Blood 110, № 7 (2007): 2685–95. http://dx.doi.org/10.1182/blood-2007-01-065870.

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We recently showed that A2A adenosine receptor activation by endogenous adenosine contributes to interleukin-10 (IL-10) production in polymicrobial sepsis. Here we investigated the molecular mechanisms underpinning this interaction between adenosine receptor signaling and infection by exposing macrophages to Escherichia coli. We demonstrated using receptor knockout mice that A2A receptor activation is critically required for the stimulatory effect of adenosine on IL-10 production by E coli–challenged macrophages, whereas A2B receptors have a minor role. The stimulatory effect of adenosine on E

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Matsunaga, Takuya, Fumio Fukai, Takuro Kameda, et al. "Potentiated Activation of VLA-4 and VLA-5 Accelerates Proplatelet-Like Formation In Megakaryocytes." Blood 116, no. 21 (2010): 2585. http://dx.doi.org/10.1182/blood.v116.21.2585.2585.

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Abstract Abstract 2585 Several lines of reports have suggested that mature magakaryocytes (MKs) form long cytoplasmic processes containing platelets (PLT) organelles from which PLT break off due to blood flow pressures in bone marrow (BM). These cytoplasmic processes were termed ‘proplatelet'. MKs differentiated from hematopoietic stem cells by in vitro culture also develop similar processes, referred to as ‘proplatelet-like formation (PPF)'. It has been already reported that fibronectin (FN) and phorbol 12-myristate 13-acetate (PMA) are essential for inducing PPF in MKs using CHRF-288 human m

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Wang, ZacK Z., Hao Bai, Melanie Arzigian, Yong-Xing Gao, and Wen-Shu Wu. "BMP4 and TGFbeta Differentially Regulate CD34+ Progenitor Development in Human Embryonic Stem Cells through SMAD-Dependent Pathway." Blood 112, no. 11 (2008): 889. http://dx.doi.org/10.1182/blood.v112.11.889.889.

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Abstract Pluripotent stem cells derived from patients, including embryonic stem (ES) cells and “induced pluripotent stem” (iPS) cells, are a promising area of regenerative medical research. A major roadblock toward human clinical therapies using ES cells or iPS cells is to define the factors that direct ES cell differentiation into lineage specific cells. We previously established a simple and efficient human embryonic stem cell (hESC) differentiation system to generate CD34+/CD31+ progenitor cells that gave rise to hematopoietic and endothelial cells (Nat Biotech.25:317, 2007). To advance pot

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Actas de conferencias sobre el tema "Hd62.4 .p38 2007"

Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α.

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