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2015 Feb. Solarewicz JZ, Angoa-Perez M, Kuhn DM, Mateika JH. DRAGO (KIAA0247), a New DNA Damage-Responsive, p53-Inducible Gene That Cooperates With p53 as Oncosupprossor. Proteomic analyses confirmed increased proteasomal activity and adaptive stress responses in muscle of Sod1-/- mice that were absent in mSod1KO mice. Hellekant G, Schmolling J, Marambaud P, Rose-Hellekant TA. J Immunol. However, when … Genetic and Pharmacological Inhibition of TREM-1 Limits the Development of Experimental Atherosclerosis. Keywords: The analogy, not meant to be taken too seriously, concerns Bill, a retired geneticist, and Doug, a retired biochemist, and their attempts to ascertain how cars work while observing a car production plant. J Neurochem. 2018. RIM-binding protein 2 regulates release probability by fine-tuning calcium channel localization at murine hippocampal synapses. Targeted disruption of the peroxisomal thiolase B gene in mouse: a new model to study disorders related to peroxisomal lipid metabolism. Nat Commun. Consistent with a critical role for GLUT4 in mediating glucose sensing in the brain, in recent work whole-body GLUT4 knockout mice showed impaired neuronal activation during hypoglycemia (B.B.K., personal communication). The sleep-wake cycle and motor activity, but not temperature, are disrupted over the light-dark cycle in mice genetically depleted of serotonin. Acceleration of collateral development by carcinoembryonic antigen-related cell adhesion molecule 1 expression on CD11b/⁺Gr-1⁺ myeloid cells--brief report. Biol Chem. Cells from idPD patients reveal a significant deficiency in store-operated PLA2G6-dependent Ca2+ signaling. Nat Genet. A whole-body KO was used as a first step as potential sites of action have not been defined and this will provide us with the opportunity to do so. Nonetheless, these results demonstrate NAD+is a key physiological regulator of thermogenic and mitochondrial genes, such as UCP1 and PGC1α, in BAT. For example, in order to study a disease that affec… 2018 Feb 1;28(4):275-295. doi: … 2011 Feb 1. Sphingosine kinase 2 deficient mice exhibit reduced experimental autoimmune encephalomyelitis: Resistance to FTY720 but not ST-968 treatments. Protein homeostasis was measured ex vivo in extensor digitorum longus by incorporation of l ‐[U‐ 14 C]phenylalanine, and metabolomic and lipidomic profiling of skeletal muscle was performed by Metabolon, Inc. Extracellular nucleotides induce migration of renal mesangial cells by upregulating sphingosine kinase-1 expression and activity. Am J Physiol Renal Physiol. Diabetologia. Adult whole-body conditional BACE1 knockout mice lack epileptiform abnormalities and hypomyelination Spontaneous seizure and abnormal EEGs are other adverse phenotypes that have been reported in BACE1-/- mice (19, 20). 2018 Feb 4. 2014 Feb 1. Normal development of mice lacking PAXX, the paralogue of XRCC4 and XLF. COX2 expression and Erk1/Erk2 activity mediate Cot-induced cell migration. Mammalian ALKBH8 possesses tRNA methyltransferase activity required for the biogenesis of multiple wobble uridine modifications implicated in translational decoding. Thiazolidinediones partially reverse the metabolic disturbances observed in Bscl2/seipin-deficient mice. Mice genetically depleted of brain serotonin do not display a depression-like behavioral phenotype. Biochimie. NIH Figure 1. 2013 Mar 6. Andreas F. Kolb, Reinhard C. Huber, Simon G. Lillico, Ailsa Carlisle, Claire J. Robinson, Claire Neil, Linda Petrie, Dorte B. Sorensen, I. Anna S. Olsson, C. Bruce A. Whitelaw. Ma Z, Siebert AP, Cheung KH, Lee RJ, Johnson B, Cohen AS, Vingtdeux V, Marambaud P, Foskett JK. In contrast to mSod1KO mice, myofiber atrophy in Sod1-/- mice was associated with increased muscle oxidative damage, neuromuscular junction degeneration, denervation, nerve demyelination, and upregulation of proteins involved in maintenance of myelin sheaths. 2015 Dec 8. Angoa-Pérez M, Herrera-Mundo N, Kane MJ, Sykes CE, Anneken JH, Francescutti DM, Kuhn DM. Generation of mice with inactivated Rh or Rhag genes. 2007 Jul. Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype. Caparrós-Martín JA, Valencia M, Reytor E, Pacheco M, Fernandez M, Perez-Aytes A, Gean E, Lapunzina P, Peters H, Goodship JA, Ruiz-Perez VL. Mestre H, Hablitz LM, Xavier AL, Feng W, Zou W, Pu T, Monai H, Murlidharan G, Castellanos Rivera RM, Simon MJ, Pike MM, Plá V, Du T, Kress BT, Wang X, Plog BA, Thrane AS, Lundgaard I, Abe Y, Yasui M, Thomas JH, Xiao M, Hirase H, Asokan A, Iliff JJ, Nedergaard M. Sakellariou GK, Davis CS, Shi Y, Ivannikov MV, Zhang Y, Vasilaki A, Macleod GT, Richardson A, Van Remmen H, Jackson MJ, McArdle A, Brooks SV. McDonagh B, Scullion SM, Vasilaki A, Pollock N, McArdle A, Jackson MJ. To determine the role of adipose tissue AMPK in vivo, we generated fat-specific AMPKα1/α2 knockout mice (AMPKFKO) using the Cre-loxP system. Imeri F, Schwalm S, Lyck R, Zivkovic A, Stark H, Engelhardt B, Pfeilschifter J, Huwiler A. CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes. All tissues and plasma in the BChE−/− mice are devoid of BChE activity. Martin J, Maurhofer O, Bellance N, Benard G, Graber F, Hahn D, Galinier A, Hora C, Gupta A, Ferrand G, Hoppeler H, Rossignol R, Dufour JF, St-Pierre MV. Mice genetically depleted of brain serotonin display social impairments, communication deficits and repetitive behaviors: possible relevance to autism. A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver. J Biol Chem. Dobbertin A, Hrabovska A, Dembele K, Camp S, Taylor P, Krejci E, Bernard V. Unique Distal Enhancers Linked to the Mouse Tnfsf11 Gene Direct Tissue-Specific and Inflammation-induced Expression of RANKL. On the mechanisms underlying attenuated redox responses to exercise in older individuals: A hypothesis. 2010 Apr;30(7):1814-27. Generation of mice with inactivated Rh or Rhag genes. They were generated by crossing mice with a floxed Bace1 gene to mice carrying a transgene encoding Cre recombinase fused to the estrogen receptor, inserted at the ROSA26 locus. Am J Physiol Renal Physiol. Chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice. Mol Cell Biol. Remarkably, these mice also showed increased insulin sensitivity in adipose tissue but not skeletal muscle, similar to the metabolic phenotypes observed in inducible whole-body knockout mice. Salty Taste Deficits in CALHM1 Knockout Mice. Nature. 2004 Dec 3. Daude N, Wohlgemuth S, Brown R, Pitstick R, Gapeshina H, Yang J, Carlson GA, Westaway D. This gene inactivation is achieved at all stages of development, from the one-cell embryo stage through adulthood. Grauel MK, Maglione M, Reddy-Alla S, Willmes CG, Brockmann MM, Trimbuch T, Rosenmund T, Pangalos M, Vardar G, Stumpf A, Walter AM, Rost BR, Eickholt BJ, Haucke V, Schmitz D, Sigrist SJ, Rosenmund C. Normal development of mice lacking PAXX, the paralogue of XRCC4 and XLF. Molecular changes in transcription and metabolic pathways underlying muscle atrophy in the CuZnSOD null mouse model of sarcopenia. Nicolas-Francès V, Arnauld S, Kaminski J, Ver Loren van Themaat E, Clémencet MC, Chamouton J, Athias A, Grober J, Gresti J, Degrace P, Lagrost L, Latruffe N, Mandard S NLM 28, 275-295. WWP1 knockout in mice exacerbates obesity-related phenotypes in white adipose tissue but improves whole-body glucose metabolism FEBS Open Bio. Whole-body Pparα −/− mice show impaired coping with prolonged fasting, resulting in defective fatty acid oxidation and steatosis, hypoglycaemia and hypothermia. CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes. J Bone Miner Res. Knockout of the prion protein (PrP)-like Sprn gene does not produce embryonic lethality in combination with PrP(C)-deficiency. 2009 Jul 1. Early glomerular filtration defect and severe renal disease in podocin-deficient mice. Genes Brain Behav. APN-KO mice had reduced body fat and decreased whole-skeleton bone mineral density. mice, indicative of defective glucose homeostasis (Figure S1J). Readers may be aware of the amusing allegories written by William Sullivan and Douglas Kellogg on the relative merits of investigating processes using genetic versus biochemical approaches . FEBS Lett. Clipboard, Search History, and several other advanced features are temporarily unavailable. BChE−/− mice have no distinguishable phenotype. 2014 Sep. Sun Y, Caplazi P, Zhang J, Mazloom A, Kummerfeld S, Quinones G, Senger K, Lesch J, Peng I, Sebrell A, Luk W, Lu Y, Lin Z, Barck K, Young J, Del Rio M, Lehar S9, Asghari V8, Lin W1, Mariathasan S9, DeVoss J1, Misaghi S10, Balazs M1, Sai T5, Haley B, Hass PE, Xu M, Ouyang W, Martin F, Lee WP, Zarrin AA Epub 2020 Sep 12. 2014 Jul. The mouse as a model for human cancer research has proven to be a useful tool due to the relatively similar genomic and physiological characteristics of tumor biology between mice and humans. Mice genetically depleted of brain serotonin do not display a depression-like behavioral phenotype. 2020 Dec;11(6):1688-1704. doi: 10.1002/jcsm.12615. … To identify the functions of PIKE in a systemic context, we generated the whole body PIKE knockout (PIKE -/-) mice using the loxP/Cre recombination that the exons 3 to 6 of the CENTG1were removed, thus introducing a shift to the original reading frame and producing a truncation in the GTPase domain of all PIKE … Genetic deletion of trace amine 1 receptors reveals their role in auto-inhibiting the actions of ecstasy (MDMA). 2012 Jul 10. Lack of Cu,Zn-superoxide dismutase (CuZnSOD) in homozygous knockout mice (Sod1-/-) leads to accelerated age-related muscle loss and weakness, but specific deletion of CuZnSOD in skeletal muscle (mSod1KO mice) or neurons (nSod1KO mice) resulted in only mild muscle functional deficits and failed to recapitulate the loss of mass and function observed in Sod1-/- mice. 2020 Mar;10(3):306-315. doi: 10.1002/2211-5463.12795. Epub 2015 Apr 15. Innovation and Conclusion: These findings demonstrate that neuromuscular integrity, redox mechanisms, and pathways are differentially altered in nerve and muscle of Sod1-/- and mSod1KO mice. To gain insights into how ACBP impinges on weaning and the concomitant remodeling of whole-body lipid metabolism we performed a comparative lipidomics analysis charting the absolute abundance of 613 lipid molecules in liver, muscle and plasma from weaning and adult Acbp knockout and wild type mice. Aims: Lack of Cu,Zn-superoxide dismutase (CuZnSOD) in homozygous knockout mice (Sod1−/−) leads to accelerated age-related muscle loss and weakness, but specific deletion of CuZnSOD in skeletal muscle (mSod1KO mice) or neurons (nSod1KO mice) resulted in only mild muscle functional deficits and failed to recapitulate the loss of mass and function observed in Sod1−/− mice.  |  A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver. Enhancement of reactive oxygen species production and chlamydial infection by the mitochondrial Nod-like family member NLRX1. Thus, to determine whole-body glucose utilization and the contributions of each insulin-targeted tissue to glucose uptake, we performed a glucose kinetics study, using the radiolabeled glucose analog (18)F-2-fluoro-2-deoxy-D-glucose ((18)F-FDG), in wild-type (WT) and SMS2 knockout (KO) mice. 2014 Nov. Angoa-Pérez M, Kane MJ, Briggs DI, Herrera-Mundo N, Sykes CE, Francescutti DM, Kuhn DM. The sleep-wake cycle and motor activity, but not temperature, are disrupted over the light-dark cycle in mice genetically depleted of serotonin. In 2-3 month-old wild type (WT) and Mapt-KO mice fed ad lib chow diet, we observed no significant difference in glucose or insulin tolerance. Epub 2020 May 12. 9 … 2016. Both male and female adult mice were used in this trial. 2009 Oct 1. Inflamm Bowel Dis. Progressive motor dysfunction in aging KO, but not in WT mice developed at an age range that aligns with that typical of idPD in humans. Milk Lacking α-Casein Leads to Permanent Reduction in Body Size in Mice. A knockout mouse, or knock-out mouse, is a genetically modified mouse (Mus musculus) in which researchers have inactivated, or " knocked out ", an existing gene by replacing it or disrupting it with an artificial piece of DNA. Follow these links if you are looking for another, Determine main functions of the gene and/or protein, Study human pathologies caused by gene inactivation or deficiency, Induce a phenotype to create a disease model or, Study specificity and/or off-target activities of drug candidate, Develop new antibodies on the target protein, Total absence of protein including all isoforms, or total absence of specific isoforms, Causes embryonic lethality in about 15% of all cases, May modify the animal physiology, adaptation and compensation mechanisms, resulting in false results, Global phenotype is the combination of different constitutions in different tissues that may lead to non-conclusive studies. MAP kinase phosphatase-2 plays a critical role in response to infection by Leishmania mexicana. read full testimonial, Director at UC San Diego School of Medicine, "genOway is the Mercedes Benz of transgenic outsourcing companies.". Taruno A, Vingtdeux V, Ohmoto M, Ma Z, Dvoryanchikov G, Li A, Adrien L, Zhao H, Leung S, Abernethy M, Koppel J, Davies P, Civan MM, Chaudhari N, Matsumoto I, Hellekant G, Tordoff MG, Marambaud P, Foskett JK. Proc Natl Acad Sci U S A. Mammary gland development is delayed in mice deficient for aminopeptidase N. 2012 Sep 7. Epub 2020 May 26. J Am Coll Cardiol. Endonuclease VIII-like 3 (Neil3) DNA glycosylase promotes neurogenesis induced by hypoxia-ischemia. Clin Exp Immunol. Prieur X, Dollet L, Takahashi M, Nemani M, Pillot B, Le May C, Mounier C, Takigawa-Imamura H, Zelenika D, Matsuda F, Fève B, Capeau J, Lathrop M, Costet P, Cariou B, Magré J. J Appl Physiol (1985). 2014 Jul 15. Targeting of acetylcholinesterase in neurons in vivo: a dual processing function for the proline-rich membrane anchor subunit and the attachment domain on the catalytic subunit. Comparison of Whole Body SOD1 Knockout with Muscle-Specific SOD1 Knockout Mice Reveals a Role for Nerve Redox Signaling in Regulation of Degenerative Pathways in Skeletal Muscle. Role of the C5a receptor (C5aR) in acute and chronic dextran sulfate-induced models of inflammatory bowel disease. Tordoff MG, Ellis HT, Aleman TR, Downing A, Marambaud P, Foskett JK, Dana RM, McCaughey SA 2019 Feb 15. Impairment of PARK14-dependent Ca(2+) signalling is a novel determinant of Parkinson's disease. USA.gov. MOSPD2 is a therapeutic target for the treatment of CNS inflammation. However, these effects appear to be secondary to the protection of these mice from HFD-induced obesity, since obesity is strongly associated with the development of hepatic steatosis. PILRα negatively regulates mouse inflammatory arthritis. PLoS One. Brain serotonin signaling does not determine sexual preference in male mice. See this image and copyright information in PMC. Komnenov D, Solarewicz JZ, Afzal F, Nantwi KD, Kuhn DM, Mateika JH. 2009 Nov-Dec. Steinmetz OM, Turner JE, Paust HJ, Lindner M, Peters A, Heiss K, Velden J, Hopfer H, Fehr S, Krieger T, Meyer-Schwesinger C, Meyer TN, Helmchen U, Mittrücker HW, Stahl RA, Panzer U. COX2 expression and Erk1/Erk2 activity mediate Cot-induced cell migration. Onal M, St John HC, Danielson AL, Pike JW. Upon administration of tamoxifen, Bace1 expression is abolished throughout the body. While conventional knockouts were first, involving animal models created with artificially impaired or eliminated genes that are applied to all the tissues of their bodies, conditional knockouts are more advanced, involving gene knockouts that only target specific tissues or organs. CALHM1 Deletion in Mice Affects Glossopharyngeal Taste Responses, Food Intake, Body Weight, and Life Span. J Natl Cancer Inst. Changes in whole body energy levels are closely linked to alterations in body weight and bone mass. Deletion of the Dual Specific Phosphatase-4 (DUSP-4) Gene Reveals an Essential Non-redundant Role for MAP Kinase Phosphatase-2 (MKP-2) in Proliferation and Cell Survival. N Yacov, P Kafri, Y Salem, O Propheta-Meiran, B Feldman, E Breitbart, I Mendel. Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Genetic depletion of brain 5HT reveals a common molecular pathway mediating compulsivity and impulsivity. Al-Mutairi MS, Cadalbert LC, McGachy HA, Shweash M, Schroeder J, Kurnik M, Sloss CM, Bryant CE, Alexander J, Plevin R. 2016 Dec 27. Resistance to diet-induced obesity and associated metabolic perturbations in haploinsufficient monocarboxylate transporter 1 mice. Would you like email updates of new search results? The first whole body GHR-KO [GH receptor (GHR) knockout mice] was developed in the Kopchick lab in 1997 and since then numerous studies have been done using the mouse model. J Biol Chem. To dissect any underlying cross-talk between motor neurons and skeletal muscle in the degeneration in Sod1-/- mice, we characterized neuromuscular changes in the Sod1-/- model compared with mSod1KO mice and examined degenerative molecular mechanisms and pathways in peripheral nerve and skeletal muscle. Thiazolidinediones partially reverse the metabolic disturbances observed in Bscl2/seipin-deficient mice. Over the past decade, in order the better understand the direct effects of GH in tissues (other than through IGF-1) numerous tissue-specific GHR-KO mouse models have been developed utilizing the Cre-loxP system. DRAGO (KIAA0247), a New DNA Damage-Responsive, p53-Inducible Gene That Cooperates With p53 as Oncosupprossor. Herein we generated GLUT6 knockout mice to determine how loss of GLUT6 affected whole body glucose homeostasis and metabolic physiology. ALKBH8-mediated formation of a novel diastereomeric pair of wobble nucleosides in mammalian tRNA. Knockout Mouse Project (KOMP) Conditional gene knockouts in mice are often used to study human diseases because many genes produce similar phenotypes in both species. When it comes to comparing conventional vs. conditional knockout methods, it helps to know the basics. 2016 Aug. Vingtdeux V, Chang EH, Frattini SA, Zhao H, Chandakkar P, Adrien L, Strohl JJ, Gibson EL, Ohmoto M, Matsumoto I, Huerta PT, Marambaud P. 2020 Aug. Estañ MC, Fernández-Núñez E, Zaki MS, Esteban MI, Donkervoort S, Hawkins C, Caparros-Martin JA, Saade D, Hu Y, Bolduc V, Chao KR, Nevado J, Lamuedra A, Largo R, Herrero-Beaumont G, Regadera J, Hernandez-Chico C, Tizzano EF, Martinez-Glez V, Carvajal JJ, Zong R, Nelson DL, Otaify GA, Temtamy S, Aglan M, Issa M, Bönnemann CG, Lapunzina P, Yoon G, Ruiz-Perez VL. Critical roles for WDR72 in calcium transport and matrix protein removal during enamel maturation. Nat Commun. Please enable it to take advantage of the complete set of features! The ciliary Evc/Evc2 complex interacts with Smo and controls Hedgehog pathway activity in chondrocytes by regulating Sufu/Gli3 dissociation and Gli3 trafficking in primary cilia. 2005 Dec. Ross AJ, May-Simera H, Eichers ER, Kai M, Hill J, Jagger DJ, Leitch CC, Chapple JP, Munro PM, Fisher S, Tan PL, Phillips HM, Leroux MR, Henderson DJ, Murdoch JN, Copp AJ, Eliot MM, Lupski JR, Kemp DT, Dollfus H, Tada M, Katsanis N, Forge A, Beales PL. "genOway is the Mercedes Benz of transgenic outsourcing companies." 2008 Feb. Panzer U, Steinmetz OM, Paust HJ, Meyer-Schwesinger C, Peters A, Turner JE, Zahner G, Heymann F, Kurts C, Hopfer H, Helmchen U, Haag F, Schneider A, Stahl RA. The conventional knockout method is also called as the simple-gene disruption method. Calcium homeostasis modulator 1 (CALHM1) is the pore-forming subunit of an ion channel that mediates extracellular Ca2+ regulation of neuronal excitability. Ventilatory long-term facilitation is evident after initial and repeated exposure to intermittent hypoxia in mice genetically depleted of brain serotonin. Glycogen storage disease type III: A novel Agl knockout mouse model. 2015 Jan 1. MAP kinase phosphatase-2 plays a critical role in response to infection by Leishmania mexicana. Human age equivalent is shown below. Biochimie. 2012 Jun 5. Deletion of the Distal Tnfsf11 RL-D2 Enhancer that Contributes to PTH-Mediated RANKL Expression in Osteoblast Lineage Cells Results in a High Bone Mass Phenotype in Mice. We previously generated a tamoxifen-inducible Arg1 deficient mouse model (Arg1-Cre) that disrupts Arg1 expression throughout the whole body and leads to lethality ≈ 2 weeks after gene disruption. 2020 Dec;42(6):1579-1591. doi: 10.1007/s11357-020-00200-5. Fasting and fed glucose concentrations were similar in BG4KO and control mice, consistent with similar baseline rates of EGP and glucose disposal. 2019 Feb 20;132:19-23. doi: 10.1016/j.freeradbiomed.2018.06.032. Disruption of the histidine triad nucleotide-binding hint2 gene in mice affects glycemic control and mitochondrial function. 2016 Jan 23. PLoS One. This gene inactivation is achieved at all stages of development, from the one-cell embryo stage through adulthood.  |  Thomas DM, Angoa Pérez M, Francescutti-Verbeem DM, Shah MM, Kuhn DM. Marble burying and nestlet shredding as tests of repetitive, compulsive-like behaviors in mice. Genetic inactivation of the laminin alpha5 chain receptor Lu/BCAM leads to kidney and intestinal abnormalities in the mouse. Aims: Define “Humanized”: Two Mouse Models Helping... Part 5: Preclinical Models in I/O – HSA/hFcRn, Part 3: Preclinical Models in I/O – BRGSF-HIS, Part 2: Preclinical Models in I/O – BRGSF. Br J Pharmacol. A constitutive Knockout mouse, also referred to as a conventional or whole-body Knockout (KO), defines a mouse model in which the target gene is permanently inactivated in the whole animal, in every cell of the organism. 2005 Oct. Mailliet F, Ferry G, Vella F, Thiam K, Delagrange P, Boutin JA. Mice have several similar anatomical, cellular, and molecular characteristics to humans that are known to have critical properties and functions in cancer. OBESITY. Impairment of PARK14-dependent Ca(2+) signalling is a novel determinant of Parkinson's disease. Intermittent hypoxia promotes recovery of respiratory motor function in spinal cord-injured mice depleted of serotonin in the central nervous system. Mammary gland development is delayed in mice deficient for aminopeptidase N. Disruption of the histidine triad nucleotide-binding hint2 gene in mice affects glycemic control and mitochondrial function. Results: The molecular impairment of PLA2G6-dependent Ca2+ signaling triggers a sequence of pathological events of autophagic dysfunction, progressive loss of dopaminergic (DA) neurons in substantia nigra pars compacta and age-dependent L-DOPA-sensitive motor dysfunction. Recessive mutations in muscle-specific isoforms of FXR1 cause congenital multi-minicore myopathy. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error. Enhancement of reactive oxygen species production and chlamydial infection by the mitochondrial Nod-like family member NLRX1. Nat Commun. Acceleration of collateral development by carcinoembryonic antigen-related cell adhesion molecule 1 expression on CD11b/⁺Gr-1⁺ myeloid cells--brief report. Additionally, the proportion of mouse genes with a human ortholog is 80% (1), th… Sphingosine kinase 1 and 2 regulate the capacity of mesangial cells to resist apoptotic stimuli in an opposing manner. 2015 Aug 31. Comparison of Whole Body SOD1 Knockout With Muscle-Specific SOD1 Knockout Mice Reveals a Role for Nerve Redox Signaling in Regulation of Degenerative Pathways in Skeletal Muscle Giorgos K Sakellariou et al. Also contributes to metabolic homeostasis through expression in other tissues and spleen ( )! Helps to know the basics 2014 Apr ; 28 ( 4 ):329. doi: 10.3390/antiox9040329 store-operated Ca2+ entry SOCE., Y Salem, O Propheta-Meiran, B Feldman, E Breitbart, I Mendel unique Distal Linked. 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