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#33670592   2021/02/18 To Up

Blue Light Induces Impaired Autophagy through Nucleotide-Binding Oligomerization Domain 2 Activation on the Mouse Ocular Surface.

In this study, we investigated the effects of blue light exposure on nucleotide-binding oligomerization domain 2 (NOD2) expression on the mouse ocular surface and evaluated the role of NOD2 activation in light-induced cell death. Mice were divided into wild-type (WT), NOD2-knock out (KO), WT + blue light (WT + BL), and NOD2-KO + blue light (NOD2-KO + BL) groups, and the mice in the WT+BL and NOD2-KO + BL groups were exposed to blue light for 10 days. After 10 days of blue light exposure, increased reactive oxygen species and malondialdehyde were observed in the WT + BL and NOD2-KO + BL groups, and the WT + BL group showed a higher expression of NOD2 and autophagy related 16 like 1. Although both WT+BL and NOD2-KO + BL groups showed an increase in the expression of light chain 3-II, NOD2-KO + BL mice had a significantly lower p62 expression than WT + BL mice. In addition, NOD2-KO+BL mice had significantly lower corneal epithelial damage and apoptosis than WT + BL mice. In conclusion, blue light exposure can induce impaired autophagy by activation of NOD2 on the ocular surface. In addition, the reactive oxygen species (ROS)-NOD2-autophagy related 16 like 1 (ATG16L) signaling pathway may be involved in the blue-light-induced autophagy responses, resulting in corneal epithelial apoptosis.
Ying Li, Rujun Jin, Lan Li, Ji Suk Choi, Jonghwa Kim, Hyeon Jeong Yoon, Jong Hwan Park, Kyung Chul Yoon

1380 related Products with: Blue Light Induces Impaired Autophagy through Nucleotide-Binding Oligomerization Domain 2 Activation on the Mouse Ocular Surface.

100ul100 ul100 ul100 ul200 25ml1.5 mg100 20ug250ul

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#33644146   2021/02/12 To Up

Survey of Candidate Single-Nucleotide Polymorphisms in SLC11A1, TLR4, NOD2, PGLYRP1, and IFNγ in Ankole Longhorn Cattle in Central Region of Uganda to Determine Their Role in Subspecies Infection Outcome.

ssp. (MAP) is the cause of Johne's disease (JD) in a wide range of domestic and wild ruminants. Single-nucleotide polymorphisms (SNPs) in several genes including solute-like carrier 11A1 (SLC11A1), interferon gamma (IFNγ), Toll-like receptor 4 (TLR4), nucleotide-binding oligomerization domain 2 gene (NOD2), and bovine peptidoglycan recognition protein 1 (PGLYRP1) have been implicated in influencing the infection outcome of MAP in cattle. We have carried out a survey in a population of Ankole cattle from three districts in the central region of Uganda including Isingiro, Lyantonde, and Rakai to determine the role played by several SNPs on the above genes in the infection outcome of local cattle in Uganda. Nine hundred fifty-five heads of cattle obtained from 93 herds were tested using ELISA. Thirty-five ELISA-positive cattle and 35 negative herd mates from a total of 955 cattle tested for MAP were genotyped using iPLEX MassARRAY genotyping systems to detect the presence of a total of 13 SNPS in five different genes (SLC11A1, IFNγ, TLR4, NOD2, and PGLYRP1). The cow-level prevalence of MAP infection in Ankole Longhorn cattle in the three districts was 3.98% (35/955), while the herd-level prevalence was 27.9% and within-herd prevalence was 12 ± 1.5% (95% CI = 9.1-14.8%). The genotypes and allele frequencies of the MAP-positive cattle were compared with those of their ELISA-negative herd mates to determine the significance of the polymorphisms. The results showed that SNPs rs109915208, rs110514940, and rs110905610 on SLC11A1, c.480G>A and c.625C>A on PGLYRP1, and c.2021C>T on TLR4 were monomorphic in both seropositive and seronegative cattle and therefore had no influence on the infection outcome. The remaining SNPs studied in the five genes [: rs109614179; : rs29017188 (c.226G>C), c.2021C>T; NOD2: rs110536091, rs111009394; : c.102G>C, c.480G>A, c.625C>A; γ: rs110853455] were polymorphic, but their allele and genotype frequencies did not show any significant difference between the seropositive and seronegative cattle. No significant difference was observed for any haplotype at the gene level.
Julius Boniface Okuni, Mathias Afayoa, Lonzy Ojok

1095 related Products with: Survey of Candidate Single-Nucleotide Polymorphisms in SLC11A1, TLR4, NOD2, PGLYRP1, and IFNγ in Ankole Longhorn Cattle in Central Region of Uganda to Determine Their Role in Subspecies Infection Outcome.

100 μg 100 UG100 μg100 μg100 μg100 μg100 μg100 μg100 μg100 μg100 μg100 μg

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#33639564   2021/02/24 To Up

Interferon-γ activated T-cell IRGM-autophagy axis in oral lichen planus.

Oral lichen planus (OLP) is an inflammatory immune disease featured by dense T-cell infiltrate and basal keratinocytes degeneration. Immunity related GTPase M (IRGM) is vital for the induction of autophagy. Our previous studies have demonstrated aberrant autophagy in OLP, however, the involvement of IRGM-autophagy axis in OLP has not yet been revealed. The expression of IRGM and autophagy activity were evaluated in oral mucosal tissues and peripheral T cells of OLP patients and healthy controls, respectively. We found significant upregulation of IRGM and LC3B in lesions of patients with OLP as compared with healthy donors. IRGM, LC3B and NOD2 levels were also elevated in the peripheral T cells of OLP. Then, knockdown of IRGM after electrotransfection with siRNA resulted in attenuated autophagy, growth inhibition, and apoptosis of T cells. In addition, preincubation with IFN-γ promoted the expression of IRGM mRNA and induced autophagy in T cells. Furthermore, IFN-γ decreased the proliferation and apoptosis of T cells, whereas facilitated the viability of keratinocytes in a co-culture system of activated T cells and keratinocytes. Taken together, activated IRGM-autophagy axis under IFN-γ regulation in T cells might participate in the immunoregulatory mechanism of OLP.
Ya-Qin Tan, Fang Wang, Rui-Jie Ma, Jing Zhang, Gang Zhou

1233 related Products with: Interferon-γ activated T-cell IRGM-autophagy axis in oral lichen planus.

1 mL96 assays100ug Lyophilized25 96 samples250ul

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#33633342   2021/02/26 To Up

Admixture/fine-mapping in Brazilians reveals a West African associated potential regulatory variant (rs114066381) with a strong female-specific effect on body mass and fat mass indexes.

Admixed populations are a resource to study the global genetic architecture of complex phenotypes, which is critical, considering that non-European populations are severely underrepresented in genomic studies. Here, we study the genetic architecture of BMI in children, young adults, and elderly individuals from the admixed population of Brazil.
Marilia O Scliar, Hanaisa P Sant'Anna, Meddly L Santolalla, Thiago P Leal, Nathalia M Araújo, Isabela Alvim, Victor Borda, Wagner C S Magalhães, Mateus H Gouveia, Ricardo Lyra, Moara Machado, Lucas Michelin, Maíra R Rodrigues, Gilderlanio S Araújo, Fernanda S G Kehdy, Camila Zolini, Sérgio V Peixoto, Marcelo R Luizon, Francisco Lobo, Michel S Naslavsky, Guilherme L Yamamoto, Yeda A O Duarte, Matthew E B Hansen, Shane A Norris, Robert H Gilman, Heinner Guio, Ann W Hsing, Sam M Mbulaiteye, James Mensah, Julie Dutil, Meredith Yeager, Edward Yeboah, Sarah A Tishkoff, Ananyo Choudhury, Michele Ramsay, Maria Rita Passos-Bueno, Mayana Zatz, Timothy D O Connor, Alexandre C Pereira, Mauricio L Barreto, Maria Fernanda Lima-Costa, Bernardo L Horta, Eduardo Tarazona-Santos

2078 related Products with: Admixture/fine-mapping in Brazilians reveals a West African associated potential regulatory variant (rs114066381) with a strong female-specific effect on body mass and fat mass indexes.

4 Membranes/Box100 2 Pieces/Box4 Arrays/Slide4 Membranes/Box2 Pieces/Box4 Membranes/Box50ug2 Pieces/Box4 Arrays/Slide2 Pieces/Box

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#33621644   2021/02/20 To Up

First report of liver transplantation in Blau syndrome: The challenges faced in this rare granulomatous liver disease.

Blau syndrome is a rare autoinflammatory granulomatous disease caused by variants in the NOD2 gene, classically presenting in childhood. Hepatic manifestations are recognized including cholestasis and granulomatous liver disease. We describe a novel NOD2 gene variant c.1471A > C, p.(Met491Leu) in an adult who developed cirrhotic complications despite selective immunotherapy, including recurrent esophageal bleeding and spontaneous bacterial peritonitis which resulted in liver transplantation. He required a second liver transplant as his first graft failed due to ischemic cholangiopathy. Disease recurrence has been observed (hitherto unreported). Of 84 patients with Blau syndrome treated with antibody therapy, five hepatic cases responded to anti-TNF therapy, with promising results if instigated before decompensation occurs. We report the first case of liver transplantation for Blau syndrome in an adult with a novel NOD2 variant. Blau related liver disease can reoccur post transplantation and is an important consideration for any future graft. LAY SUMMARY: Blau syndrome is a rare immune disease which presents in childhood. We describe the first liver transplant for this condition following development of progressive liver disease in adulthood. The patient had a newly described variant in the Blau gene (NOD2). We discuss the effectiveness of antibody therapy currently being used to control the disease, and the role of liver transplantation in Blau syndrome.
Ricky Sinharay, Lorcán McKeown, Catriona Phillips, Alice Li, Adam Duckworth, Frances Hall, William J H Griffiths

1047 related Products with: First report of liver transplantation in Blau syndrome: The challenges faced in this rare granulomatous liver disease.

96 wells

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#33609614   2021/02/17 To Up

Identification and functional analysis of NOD2 and its two splicing variants associated with a novel pattern of signal regulation in teleost fishes.

The nucleotide-binding oligomerization domain 2 (NOD2) has been identified as an important sensor for microorganic invasion in both mammals and teleost fishes. In this study, two splicing variants of NOD2 (NOD2-v1 and NOD2-v2) were identified as truncating the functional domains of wild-type NOD2 in the teleost fish Schizothorax prenanti. NOD2-v1 included an intron sequence that terminated within the third leucine-rich repeat (LRR) domain, while NOD2-v2 incorporated an insertion of one and half intron sequences and truncated within the second caspase activation and recruitment domain (CARD). NOD2, NOD2-v1 and NOD2-v2 genes were ubiquitously expressed. All three genes positively responded to exposure of Aeromonas hydrophila and lipopolysaccharide stimulation in varying degrees. Using luciferase activity assays in HEK293T cells, our results revealed that NOD2 activated the NF-κB signal and recognized muramyl dipeptide (MDP). NOD2-v1 exhibited deficiency in the LRR domains and could not sense MDP, but maintained the ability to activate NF-κB and enhanced NOD2-mediated MDP recognition. Given the significant change to the functional structure, NOD2-v2 lost its capacity for NF-κB activation, but interestingly repressed NOD2-mediated MDP sensing and NF-κB activation, and even NOD2-v1-induced NF-κB activation. Altogether, our study reveals a novel pattern of signal regulation by splicing variants in teleost fishes.
Yunkun Li, La Jin, Puzhen Xia, Weikai Sui, Anqi Huang, Guixian Bu, Fengyan Meng, Fanli Kong, Xiaohan Cao, Xingfa Han, Guozhi Yu, Xiaofu Pan, Shiyong Yang, Chongquan Zheng, Xianyin Zeng, Xiaogang Du

1286 related Products with: Identification and functional analysis of NOD2 and its two splicing variants associated with a novel pattern of signal regulation in teleost fishes.

200ug10 mg100 mg300 units10 mg2.5 mg2 Pieces/Box1 mg100 μg100ug1,000 tests

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#33609010   2021/02/19 To Up

Novel chimeric TLR2/NOD2 agonist CL429 exhibited significant radioprotective effects in mice.

Severe ionizing radiation causes the acute lethal damage of haematopoietic system and gastrointestinal tract. Here, we found CL429, the novel chimeric TLR2/NOD2 agonist, exhibited significant radioprotective effects in mice. CL429 increased mice survival, protected mice against the lethal damage of haematopoietic system and gastrointestinal tract. CL429 was more effective than equivalent amounts of monospecific (TLR2 or NOD2) and combination (TLR2 + NOD2) of molecules in preventing radiation-induced death. The radioprotection of CL429 was mainly mediated by activating TLR2 and partially activating NOD2. CL429-induced radioprotection was largely dependent on the activation of TLR2-MyD88-NF-κB signalling pathway. In conclusion, the data suggested that the co-activation of TLR2 and NOD2 could induce significant synergistic radioprotective effects and CL429 might be a potential high-efficiency selective agent.
Ying Cheng, Jicong Du, Ruling Liu, Suhe Dong, Jianming Cai, Fu Gao, Cong Liu

1426 related Products with: Novel chimeric TLR2/NOD2 agonist CL429 exhibited significant radioprotective effects in mice.

300 units100 μg100.00 ug100 μg25 mg100 μg10024 tests 1 G100ug Lyophilized

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#33602264   2021/02/18 To Up

A novel mutation in early-onset sarcoidosis/Blau syndrome: an association with Propionibacterium acnes.

Early-onset sarcoidosis (EOS) and Blau syndrome (BS) are systemic inflammatory granulomatous diseases without visible pulmonary involvement, and are distinguishable from their sporadic and familial forms. The diseases are characterized by a triad of skin rashes, symmetrical polyarthritis, and recurrent uveitis. The most common morbidity is ocular involvement, which is usually refractory to conventional treatment. A gain-of-function mutation in the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) gene has been demonstrated in this disease; however, little is known about the relationship between the activation of NOD2 and the pathophysiology of EOS/BS. Here we describe EOS/BS with a novel mutation in the NOD2 gene, as well as detection of Propionibacterium acnes (P. acnes) in the granulomatous inflammation.
Fumiko Okazaki, Hiroyuki Wakiguchi, Yuno Korenaga, Tamaki Nakamura, Hiroki Yasudo, Shohei Uchi, Ryoji Yanai, Nobuyuki Asano, Yoshinobu Hoshii, Tsuyoshi Tanabe, Kazushi Izawa, Yoshitaka Honda, Ryuta Nishikomori, Keisuke Uchida, Yoshinobu Eishi, Shouichi Ohga, Shunji Hasegawa

2492 related Products with: A novel mutation in early-onset sarcoidosis/Blau syndrome: an association with Propionibacterium acnes.

100 μg100ug100 μg100ug Lyophilized100.00 ul 100ul100 μg0.1 mg100 μg

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#33601309   2021/02/03 To Up

Design of pyrido[2,3-d]pyrimidin-7-one inhibitors of receptor interacting protein kinase-2 (RIPK2) and nucleotide-binding oligomerization domain (NOD) cell signaling.

Receptor interacting protein kinase-2 (RIPK2) is an enzyme involved in the transduction of pro-inflammatory nucleotide-binding oligomerization domain (NOD) cell signaling, a pathway implicated in numerous chronic inflammatory conditions. Herein, a pyrido[2,3-d]pyrimidin-7-one based class of RIPK2 kinase and NOD2 cell signaling inhibitors is described. For example, 33 (e.g. UH15-15) inhibited RIPK2 kinase (IC = 8 ± 4 nM) and displayed > 300-fold selectivity versus structurally related activin receptor-like kinase 2 (ALK2). This molecule blocked NOD2-dependent HEKBlue NF-κB activation (IC = 20 ± 5 nM) and CXCL8 production (at concentrations > 10 nM). Molecular docking suggests that engagement of Ser25 in the glycine-rich loop may provide increased selectivity versus ALK2 and optimal occupancy of the region between the gatekeeper and the αC-helix may contribute to potent NOD2 cell signaling inhibition. Finally, this compound also demonstrated favorable in vitro ADME and pharmacokinetic properties (e.g. C = 5.7 μM, T = 15 min, t = 3.4 h and Cl = 45 mL/min/kg following single 10 mg/kg intraperitoneal administration) further supporting the use of pyrido[2,3-d]pyrimidin-7-ones as a new structure class of RIPK2 kinase and NOD cell signaling inhibitors.
Sameer Nikhar, Ioannis Siokas, Lisa Schlicher, Seungheon Lee, Mads Gyrd-Hansen, Alexei Degterev, Gregory D Cuny

1103 related Products with: Design of pyrido[2,3-d]pyrimidin-7-one inhibitors of receptor interacting protein kinase-2 (RIPK2) and nucleotide-binding oligomerization domain (NOD) cell signaling.

200ul100ul2 Pieces/Box7 inhibitors96T50ug100μg96T200ul100ug Lyophilized8 inhibitors

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#33580557   2021/02/12 To Up

Receptor-interacting protein kinase 2 contributes to host innate immune responses against Fusobacterium nucleatum in macrophages and decidual stromal cells.

Chorioamnionitis is caused by a bacterial infection that ascends from the vagina and can cause adverse pregnancy outcomes (APOs). Fusobacterium nucleatum (F. nucleatum) is a periodontal pathogen associated with the occurrence of APOs. In this study, we evaluated whether receptor-interacting protein kinase 2 (Ripk2), an adaptor protein of the cytosolic receptors NOD1 and NOD2, in macrophages and human decidual stromal cells (hDSCs) contributes to immune responses against F. nucleatum.
Ji-Yeon Park, Tae-Sung Lee, Eui Jeong Noh, Ah-Ra Jang, Jae-Hun Ahn, Dong-Yeon Kim, Do-Hyeon Jung, Eun-Jung Song, Yeon-Ji Lee, Yun-Ji Lee, Sung Ki Lee, Jong-Hwan Park

1839 related Products with: Receptor-interacting protein kinase 2 contributes to host innate immune responses against Fusobacterium nucleatum in macrophages and decidual stromal cells.

200ul100ug Lyophilized200ul100ug Lyophilized50ul100 100ug Lyophilized100ug Lyophilized1 mg100200ul

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