Naringin alters the cholesterol biosynthesis and antioxidant enzyme activities in LDL receptor-knockout mice under cholesterol fed condition. Life Sci. 2004 Feb 13; 74(13):1621-34 ...
Many neurotransmitters, hormones and sensory stimuli elicit their cellular responses through the targeted activation of receptors coupled to Gq family heterotrimeric G proteins. Nevertheless, we still understand little about the consequences of loss of this signaling activity on brain function. We therefore examined the effects of genetic inactivation of Gnaq on responsiveness in a battery of behavioral tests in order to assess the contribution of Gaq signaling capacity in the brain circuits mediating expression of affective behaviors (anxiety and behavioral despair), spatial working memory and locomotor output (coordination, strength, spontaneous activity and drug-induced responses). First, we replicated and extended findings showing clear motor deficits in Gaq knockout mice as assessed on an accelerating rotarod and the inverted screen test. We then assessed the contribution of the basal ganglia motor loops to these impairments, using open field testing and analysis of drug-induced locomotor
15-Lipoxygenase-2 (ALOX15B), an oxidoreductase in the metabolism of arachidonic acid, is a functional tumor suppressor whose expression is reduced in a variety of human cancers. To determine the roles of ALOX15B in carcinogenesis, we generated transgenic mice with ALOX8, the murine homolog of ALOX15B, knocked out. ALOX8 expression at mRNA level was abolished in homozygous knockout mice and reduced to half of wild type in heterozygous knockout mice. Its observed that homozygous female ALOX8 knockout mice are infertile but male ALOX8 knockout mice are fertile. Increased incidence of tumor as uni or multimass was found in the lung, prostate and in the mesentery region of homozygous and heterozygous ALOX8 knockout mice, when compared with little mate wild type mice. Histological evaluations showed an increase in secondary tumors and inflammation in different tissues like lung and large intestine in mice with ALOX8 knocked out. The transgenic mice could be a good model to study the role of ...
Our results show an important role for the extracellular matrix molecule TN-C in the regulation of neural precursor cell proliferation and migration, as revealed by reduced proliferation of SVZ cells and OP cells in transgenic mice that lack TN-C (Saga et al., 1992). These mice have previously been reported as normal (Saga et al., 1992). Although subsequent studies have revealed changes in behaviour (Fukamauchi et al., 1996; Kiernan et al., 1999) and neurotransmitter levels (Fukamauchi et al., 1996) in the CNS, as well as abnormalities of neuromuscular junction architecture (Cifuentes-Diaz et al., 1998) and repair in the kidney (Nakao et al., 1998), no developmental abnormalities have been described previously. Our results are therefore important in that they demonstrate for the first time a significant role for TN-C in the basic processes of cell growth control during normal development.. The reduction in cell proliferation in the TN-C-deficient animals was revealed by BrdU studies in vivo, ...
There is growing evidence that neuropeptide Y acting through Y1 and Y2 receptors has a prominent role in modulating anxiety- and depression-like behavior in rodents. However, a role of other Y receptors like that of Y4 receptors in this process is poorly understood. We now investigated male Y2, Y4 single and Y2/Y4 double knockout mice in behavioral paradigms for changes in motor activity, anxiety and depression-like behavior. Y4 and Y2 knockout mice revealed an anxiolytic phenotype in the light/dark test, marble-burying test and motor-activity independent in stress-induced hyperthermia, and reduced depression-like behavior in the forced swim and tail suspension tests. In Y2/Y4 double knockout mice, the response in the light/dark test and in the forced swim test was further enhanced compared to Y4 and Y2 knockout mice, respectively. Motor activity was increased in Y2, Y4 and Y2/Y4 knockout mice under changing and stressful conditions, but not altered in a familiar environment. High levels of Y4 ...
Activation of neuropeptide S (NPS) signaling has been found to produce arousal, wakefulness, anxiolytic-like behaviors, and enhanced memory formation. In order to further study physiological functions of the NPS system, we generated NPS precursor knockout mice by homologous recombination in embryonic stem cells. NPS-/- mice were viable, fertile, and anatomically normal, when compared to their wild-type and heterozygous littermates. The total number of NPS neurons-although no longer synthesizing the peptide - was not affected by the knockout, as analyzed in NPS-/- /NPSEGFP double transgenic mice. Analysis of behavioral phenotypes revealed significant deficits in exploratory activity in NPS-/- mice. NPS precursor knockout mice displayed attenuated arousal in the hole board test, visible as reduced total nose pokes and number of holes inspected, that was not confounded by increased repetitive or stereotypic behavior. Importantly, long-term memory was significantly impaired in NPS-/- mice in the ...
We have previously reported the TCR inhibitory molecule CD5 impairs reactivity of tumor-specific PBL-derived T-cell clones against the cognate target and controls their susceptibility to activation-induced cell death (AICD) triggered by tumor cells. In this report, we compared the antitumor T-cell response developed against the B16F10 melanoma engrafted in CD5-deficient and wild-type (wt) C57BL/6 mice. Our results indicate that CD5 knock out mice elicit a delayed tumor growth as compared to wt mice, which is associated with tumor infiltration by more activated tumor-reactive T lymphocytes. Our data also indicate that tumor suppression in CD5-deficient mice is transient and that tumor flare up correlates with increase in AICD of tumor-infiltrating CD8+ T cells. Our data suggest that tumor T lymphocyte infiltration occurs at early stages of cancer development and that tumor-mediated AICD is most likely involved in the induction of T-cell tolerance to malignant cells. ...
M1 Muscarinic Receptor Knockout: support involvement in cognitive processes.. The five Muscarinic Acetylcholine (ACh) receptors are G-protein coupled receptors (M1R-M5R). M1R, M3R and M5R selectively couple to Gq/G11; M2R and M4R selectively couple to Gi/Go. M1R knockout mice are viable and fertile, and have no major morphological abnormalities.. M1 muscarinic receptors are located in higher brain regions of the central nervous system that are involved in cognitive processes. Studies in M1R knockout mice show that M1 receptors may be involved in cortical memory functions that require interactions between the cerebral cortex and hippocampus. Supporting a role for M1 receptor activation in cognition, muscarinic agonist-induced activation of the MAPK pathway, which plays an important role in synaptic plasticity and many cognitive functions, is virtually abolished in primary cortical cultures or CA1 hippocampal pyramidal neurons in M1R knockout mice. ...
TY - JOUR. T1 - Phospholipase β4-knockout mouse exhibits retinal phenotype. AU - Jiang, Huiping. AU - Lyubarsky, A.. AU - Vardi, N.. AU - Pugh Jr, Edward N. AU - Chen, J.. AU - Xu, J.. AU - Simon, M. I.. AU - Wu, Dianqing. PY - 1996/2/15. Y1 - 1996/2/15. N2 - Purpose: Determine if PLC-β4 has a retinal function by making/assessing a mouse knockout. Rationale: PLC-β4 is one of the four PLC-β isoforms that have been cloned and can be activated by the Gα subunits of G-proteins of the Gq class, but not by the Gβγ subunits. PLC-β4 shares a closer homology to the NorpA protein (which mediates phototransduction in Drosopnila) than to the isoforms PLC-β1-β3. Previous immunohistochemical studies have shown that PLC-β4 is expressed in cone photoreceptors, and in bipolar and ganglion cells1. Method: A mouse line was generated in which the PLC-β4 genes are disrupted. Retinal rod function was assessed with single-flash a- and b-wave electroretinography. Anatomical analysis of rod density, rod ...
Its not every day that you get something useful at no charge. But if youre a researcher studying genes that produce secreted and transmembrane proteins, today is your day. A full 472 knockout mouse lines - all extensively characterized (phenotyped) - are now publicly available from the National Institutes of Healths Mutant Mouse Regional Resource Center (MMRRC) at the University of California, Davis. Distribution of the lines is supported by the National Center for Research Resources (NCRR) and the NIH-funded Knockout Mouse Project (KOMP) repository, operated by UC Davis and the Childrens Hospital Oakland Research Institute in Oakland, Calif. Knockout mouse lines have served as valuable models to study a range of human conditions, from obesity and heart disease to diabetes and substance abuse. In knockout laboratory mice, researchers have inactivated, or knocked out, a gene with an artificial piece of DNA. This helps scientists infer what a gene normally does by understanding what goes ...
Author: Ebinger, M. et al.; Genre: Journal Article; Published in Print: 2005-09; Title: Is testosterone a substrate of P-glycoprotein in abcb1ab knock out mice?
TY - JOUR. T1 - Mamu-A*01/Kb transgenic and MHC Class I knockout mice as a tool for HIV vaccine development. AU - Li, Jinliang. AU - Srivastava, Tumul. AU - Rawal, Ravindra. AU - Manuel, Edwin. AU - Isbell, Donna. AU - Tsark, Walter. AU - La Rosa, Corinna. AU - Wang, Zhongde. AU - Li, Zhongqi. AU - Barry, Peter A. AU - Hagen, Katharine D.. AU - Longmate, Jeffrey. AU - Diamond, Don J.. PY - 2009/4/25. Y1 - 2009/4/25. N2 - We have developed a murine model expressing the rhesus macaque (RM) Mamu-A*01 MHC allele to characterize immune responses and vaccines based on antigens of importance to human disease processes. Towards that goal, transgenic (Tg) mice expressing chimeric RM (α1 and α2 Mamu-A*01 domains) and murine (α3, transmembrane, and cytoplasmic H-2Kb domains) MHC Class I molecules were derived by transgenesis of the H-2KbDb double MHC Class I knockout strain. After immunization of Mamu-A*01/Kb Tg mice with rVV-SIVGag-Pol, the mice generated CD8+ T-cell IFN-γ responses to several known ...
Nmu (Neuromedin U) and Nmus (Neuromedin S) gene double knock-out mice. Nmu KO: Exon 9 of the Nmu gene was replaced with a PGK-neo cassette. Homozygous mutant mice show a increased body weight. Nms KO: Exon 8 of the Nms gene was replaced with a neo cassette. Homozygous mutant mice show no obvious abnormality. Nmu gene knockout mice (RBRC04549), Nms gene knockout mice (RBRC04550 ...
In humans, there are over 400 genetic syndromes that include a hearing loss component, but most of the genes underlying hearing loss syndromes are currently unknown. The knockout mice tested so far in this study represented only about 15 percent of mouse genes, so the researchers estimate that if the entire genome is searched there will be at least 450 genes required for hearing function.. Professor Steve Brown, senior author on the paper and director of British Medical Research Councils Harwell laboratory, said: Importantly, the large number of hearing loss genes identified in this study demonstrates that there are many more genes involved in deafness in mouse and human genomes than we had previously realised.. Our findings identify 52 genes that have previously not been recognised as being critical for hearing. These increase our knowledge of the many genes and molecular mechanisms required for hearing, and also provide a shortlist of new genes to investigate to discover the genetic basis ...
If one parent is a wild-type mouse and the other is a homozygous knockout mouse, their offspring will be heterozygous at the knockout gene. The mouse will likely produce the protein from the wild-type copy of the gene, but depending on how the gene is regulated it is likely that expression of the protein will be below wild-type levels ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Approach and Results-We bred the macrophage-specific L13a knockout mice L13a Flox+/+ Cre+/+ onto apolipoprotein E-deficient background and generated the experimental double knockout mice L13a Flox+/+ Cre+/+ apolipoprotein E deficient (apoE−/−). L13a Flox+/+ Cre−/− mice on apolipoprotein E-deficient background were used as controls. Control and knockout mice were subjected to high-fat diet for 10 weeks. Evaluation of aortic sinus sections and entire aorta by en face showed significantly higher atherosclerosis in the knockout mice. Severity of atherosclerosis in knockout mice was accompanied by thinning of the smooth muscle cell layer in the media, larger macrophage area in the intimal plaque region and higher plasma levels of inflammatory cytokines. In addition, macrophages isolated from knockout mice had higher polyribosomal abundance of several target mRNAs, thus showing defect in translation control.. ...
Recent Publications. Hill S, Deepa SS, Sataranatarajan K, Premkumar P, Pulliam D, Liu Y, Soto VY, Fischer KE, Van Remmen H. Sco2 deficient mice develop increased adiposity and insulin resistance. Mol Cell Endocrinol. 2017 Nov 5;455:103-14. PMCID:PMC5592144. Sakellariou G, McDonagh B, Porter H, Giakoumaki I, Earl K, Nye G, Vasilaki A, Brooks S, Richardson A, Van Remmen H, McArdle A, Jackson MJ. 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. Antioxid Redox Signal. 2017 Oct 25. PMID: 29065712. Zhang N, Valentine JM, Zhou Y, Li ME, Zhang Y, Bhattacharya A, Walsh ME, Fischer KE, Austad SN, Osmulski P, Gaczynska M, Shoelson SE, Van Remmen H, Chen HI, Chen Y, Liang H, Musi N. Sustained NFκB inhibition improves insulin sensitivity but is detrimental to muscle health. Aging Cell. 2017 Aug;16(4):847-58. PMCID:PMC5506420. Selected Publications. Masser DR, Clark NW, Van Remmen ...
The ability to genetically modify mice is a powerful tool used in basic and applied research with many applications for the study of gene function and human disease. A current world-wide initiative is generating a knockout mouse strain for every protein coding gene using embryonic stem (ES) cells. Mouse strains and ES cells from these initiatives are made available to the worldwide research community via public repositories.. Once phenotyped, mouse models provide invaluable insights into human gene function with wide-ranging clinical implications, including better understanding of diseases and discovering gene targets for therapeutic agents.. The Embryonic Stem (ES) cell to Mouse (ES2M) service is a core APN facility which provides ready access to the global initiative to discover functional insight for every gene by generating and systematically phenotyping 20,000+ knockout mouse strains. The ES2M service enables Australian researchers to choose the genetically modified ES cell line(s) or mice ...
Sakellariou, GK,McDonagh, B,Porter, H,Giakoumaki, II,Earl, KE,Nye, GA,Vasilaki, A,Brooks, SV,Richardson, A,Van Remmen, H,McArdle, A,Jackson, MJ (2018) 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. Antioxidants & Redox Signaling, 28 :275-295 [DOI] [Details] ...
PTK787 2HCl and -7 (Lakhani et al. 2006 offers contributed to your knowledge of the physiological tasks of the caspases significantly. Oddly enough C57BL/6 mice deficient for both caspase-3 and -7 perish shortly after delivery while mice missing only caspase-3 or -7 have a normal life span and display a limited apoptotic phenotype in this genetic background (Lakhani et al. 2006 Leonard et al. 2002 This points to the functional redundancy between caspase-3 and -7 during embryogenesis. However several observations suggest that this overlap is not complete and that caspase-3 and -7 also fulfill non-redundant roles in apoptosis. For instance eye lenses of caspase-7 knockout mice are grossly normal whereas those of caspase-3 deficient mice display marked cataracts at the anterior lens pole (Zandy et al. 2005 Further support for this notion stems from biochemical studies demonstrating that caspase-3 and -7 exhibit differential activities toward multiple protein substrates with caspase-7 being more ...
J. K. White, Gerdin, A. - K. , Karp, N. A. , Ryder, E. , Buljan, M. , Bussell, J. N. , Salisbury, J. , Clare, S. , Ingham, N. J. , Podrini, C. , Houghton, R. , Estabel, J. , Bottomley, J. R. , Melvin, D. G. , Sunter, D. , Adams, N. C. , Tannahill, D. , Logan, D. W. , Macarthur, D. G. , Flint, J. , Mahajan, V. B. , Tsang, S. H. , Smyth, I. , Watt, F. M. , Skarnes, W. C. , Dougan, G. , Adams, D. J. , Ramirez-Solis, R. , Bradley, A. , and Steel, K. P. , Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes., Cell, vol. 154, no. 2, pp. 452-64, 2013. ...
In previous studies using a Cdc42GAP knockout, Cdc42 gain-of-activity mouse model, we have shown that constitutively increased Cdc42-GTP species can lead to defective hematopoietic stem/progenitor survival, adhesion, and actin cytoskeleton that may contribute to an engraftment defect in hematopoietic stem/progenitors.20 Cdc42GAP−/− mice also displayed mild anemia and deficiencies in erythroid progenitors. While this animal model provides valuable information for a possible involvement of Cdc42 activity in hematopoiesis, there are inherent weaknesses of the gain-of-activity approach that complicate interpretation of the data as they relate to the physiologic role of Cdc42. For example, this animal model cannot reveal the requirement of Cdc42 in hematopoiesis nor rebut a valid criticism that Cdc42GAP knockout may also bring about Cdc42-independent effects.. To understand the physiological role of Cdc42, we have recently generated a Cdc42-conditional knockout mouse model that uses the loxP/Cre ...
PMID: 32653576 Open Access Edmunds Lia R, Xie Bingxian, Mills Amanda M, Huckestein Brydie R, Undamatla Ramya, Murali Anjana, Pangburn Martha M, Martin James, Sipula Ian, Kaufman Brett A, Scott Iain, Jurczak Michael J (2020) Mol Metab Abstract: PARKIN is an E3 ubiquitin ligase that regulates mitochondrial quality control through a process called mitophagy. Recent human and rodent studies suggest that loss of hepatic mitophagy may occur during the pathogenesis of obesity-associated fatty liver and contribute to changes in mitochondrial metabolism associated with this disease. Whole-body Prkn knockout mice are paradoxically protected against diet-induced hepatic steatosis; however, liver-specific effects of Prkn deficiency cannot be discerned in this model due to pleotropic effects of germline Prkn deletion on energy balance and subsequent protection against diet-induced obesity. We therefore generated the first liver-specific Prkn knockout mouse strain (LKO) to directly address the role of hepatic ...
FUNCTION: This gene encodes a member of the Eph receptor family of receptor tyrosine kinase transmembrane glycoproteins. These receptors consist of an N-terminal glycosylated ligand-binding domain, a transmembrane region and an intracellular kinase domain. The encoded receptor preferentially binds membrane-bound ephrin-B ligands and is involved in nervous system and vascular development. This gene is used as a marker of intestinal stem cells. Homozygous knockout mice for this gene exhibit impaired axon guidance and vestibular function. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Aug 2015 ...
abuse advanced analyzed anesthetized animals array axial bore brain breed cerebellum chemical choline codes coil college concentrated concentrations conditions cone console control coronal correction cortex coverage critical dashed debate decades decrease decreased details differ discovery disorders displayed distribution dysfunction emergency enzyme even experiment expression flow function functions future gene generated genetics glutamate grant head health heterozygous horizontal human hypothalamic hypothalamus identified in vivo indicate investigated investigation involvement john knock knockout laboratory lack least likely listed localized loss major male many marker math matrix medical medicine mental mice might monitoring mouse neurobiology neurological neuronal neurons neuropsychiatric nose nuclei numerous orientations peak period physiological plays positioning preparation presently press proton psychiatric quadrature radiological radiology rare rather reasons recently reed regulation ...
Caspr3-Deficient Mice Exhibit Low Motor Learning during the Early Phase of the Accelerated Rotarod Task. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Estrogen Receptor-α Knock-Out Mouse Model is an eagle-i resource of type Mus musculus at Charles Drew University of Medicine and Science.
We offer a unique portfolio of transporter humanized and knockout mouse models which can be used for different in vivo applications.
Hus1 inactivation results in abnormal accumulation of γH2AX on autosomes, an extended sex body domain, inclusion of autosomes within the sex body, and X-autoso
The goal of this RFA is to produce the largest number of null mutants possible for the dollars available. NIH recognizes that the dollar figure given in the RFA will demand applicants to propose very aggressive programs that minimize cost while still providing a quality product. We aim to maximize the use of NIH dollars and intend to fund a balanced program that may include a set of applications performing different types of knockout mutations in order to cover as much of the genome as possible with the dollars available. Applicants should propose the best approach they can for accomplishing the goals of maximizing the number of null mutations, cost reduction and quality. The actual balance of the program and costs per knockout will be determined as a result of peer review, Council discussion and staff negotiation with the applicants before funding ...
FUNCTION: This gene encodes a member of the DnaJ or Hsp40 (heat shock protein 40 kD) family of proteins. The encoded protein is a molecular chaperone that stimulates the ATPase activity of Hsp70 heat-shock proteins in order to promote protein folding and prevent misfolded protein aggregation. The encoded protein may also inhibit apoptosis. Peritoneal macrophages derived from homozygous knockout mice for this gene exhibit impaired heat tolerance. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Apr 2015 ...
Albinism is the best-known of a group of rare genetic disorders that can affect both eyes and skin. Some genes have been identified that are linked to these conditions, but many remain mysterious. Now a team led by UC Davis researchers has identified dozens of these genetic mutations in a screen of gene-targeted knockout mice. The authors hope the work, published Aug. 1 in Scientific Reports, will be a resource for clinicians specializing in genetic disorders.. This mouse data may be of interest to clinicians, especially for patients with no known genetic cause for their condition, said Ala Moshiri, associate professor of ophthalmology in the UC Davis School of Medicine and corresponding author on the paper.. Skin, eyes and nerve tissue are linked because they all develop from the same early embryonic tissue. Another group of rare eye and skin disorders distinct from albinism, called phakomatoses, are also caused by genetic alterations inherited from parents or that occur by accident early ...
Genetic exploration of novel behavioral phenotypes in interleukin-7 and interleukin-18 receptor knockout mice. by Amy F. Eisener-Dorman full download exe or rar online without authorization for free.
Fast delivery of LRRC8B knockout Human Cell Lines for the study of gene function. Created by CRISPR/Cas9 genome editing. Includes matched wildtype control.
Fast delivery of DNMT3B knockout Human Cell Lines for the study of gene function. Created by CRISPR/Cas9 genome editing. Includes matched wildtype control.
Key Points. Endothelial Bmp6 conditional knockout mice exhibit hemochromatosis, whereas hepatocyte and macrophage Bmp6 conditional knockout mice do not.Our data
Safe Knockout to generate both conventional and tissue-specific Knockout mice from a single project, and substantially save time and cost.
Accelerate your research with custom-engineered knockout mouse models. Design your own conditional and constitutive knockout mice or use existing strains.
MyD88-dependent signaling in myo-/fibroblasts (MFs) is involved in epithelial barrier restoration and tolerance. However, the role of MyD88-dependent signaling by MFs in the regulation of inflammatory responses by macrophages in the colonic mucosa is poorly understood. Because colonic MFs respond to MyD88 activation with production of molecules involved in the regulation of macrophages (PGE2, PD-L1, etc.), we hypothesize that MF mediated MyD88 signaling regulates inflammatory responses from macrophages in the colon. Tamoxifen inducible Col1α2Cre Myd88 floxed mice (fibroblast and myofibroblast-specific MyD88 deletion) and α-SMACre MyD88 floxed mice (myo-fibroblast and smooth muscle cell-specific MyD88 deletion) on the same genetic background (C57BL/6) were used in this study. We observed that deletion of MyD88 within MFs resulted in the inflammatory changes and infiltration of lymphocytes within colonic mucosa and moderately aggravated DSS induced acute colitis. Activation of the lymphocyte ...
Approach and Results-SR-BI/LDLR double knockout and control LDLR knockout mice were fed atherogenic diets containing different amounts of fat, cholesterol, and sodium cholate. Double knockout mice fed atherogenic diets high in cholesterol exhibited significantly reduced survival compared with LDLR knockout mice fed the same diets. In addition to increased diet-accelerated aortic sinus atherosclerosis, we observed significant diet-induced CA atherosclerosis in double knockout mice and diet-dependent accumulation of platelets in CA atherosclerotic plaques. This was accompanied by substantial myocardial fibrosis in double knockout mice fed high cholesterol diets. Atherogenic diet fed double knockout mice also exhibited higher circulating cytokine levels, monocytosis with increased proportions of Ly6Chi and Ly6Cint monocytes, and higher adhesion molecule expression in CA endothelial cells compared with control LDLR knockout mice.. ...
Background and aims: Perilipin1 (PLIN1), a lipid droplet-associated protein, plays an important role in the regulation of lipolysis and lipid storage in adipocytes. PLIN1 has recently been reported to be expressed in macrophages within atheroma plaques, suggesting PLIN1 may play a role in the accumulation of lipids at the arterial wall and in the development of atherosclerosis. To clarify the role of PLIN1 in the pathophysiology of atherosclerosis, we assessed the progression of atherosclerosis in PLIN1 transgenic mice (Plin1Tg). Methods: Plin1Tg were crossed with apolipoprotein E knockout mice (ApoeKO). C57BL/6J mice, ApoeKO and Plin1Tg/ApoeKO received a normal chow diet for 20 weeks. Body weight, gonadal fat mass and plasma lipid concentrations were measured. Aortas were collected for quantification of atheroma lesions and histological analysis by Oil Red O staining. Results: Body weight, gonadal adipose mass and plasma triglyceride concentrations were not significantly different among the ...
Glyoxalase 1 (Glo1) is the first enzyme involved in glutathione-dependent detoxification of methylglyoxal, eventually generating D-lactate by the second enzyme glyoxalase 2 (Glo2). An accumulation of intracellular glyoxal and methylglyoxal leads to protein malfunction and mutation via formation of the advanced glycation end products (AGEs). Studies on mouse behavior suggest that methylglyoxal has anxiolytic properties. In this report, we generated and characterized a mouse knockout for Glo1. The knockout mice were viable without a pronounced phenotypic defect. Increased level of AGEs in Glo1 knockout mice was detected by immunoblotting with anti-MGH1 in liver homogenate, but not in brain. Alterations in behavior were observed in open field, light-dark transition, and tail suspension test. Open field data indicate increased exploration for novel environment and entry/stay in center zone in Glo1 knockout mice. In addition, increased light-dark transition and immobility was observed in the knockout ...
Mice with homologous disruption of the interferon gamma (IFN-gamma) gene on the C57BL/6 background were infected with Leishmania major and the immune response assessed. In contrast to wild-type or heterozygous knockout mice, deficient animals were unable to restrict growth of the parasite and suffered lethal infection over 6-8 wk. Although wild-type and heterozygous littermates developed CD4+ cells that contained transcripts for IFN-gamma and lymphotoxin, typical of T helper type 1 (Th1) cells, the knockout mice developed CD4+ cells that contained transcripts for interleukin 4 (IL-4), IL-5, and IL-13, typical of Th2 cells. ELISPOT assays confirmed the reciprocal patterns of IFN-gamma or IL-4 production by T cells in similar frequencies in the respective groups of mice, and antibody analysis confirmed the presence of Th2-mediated isotype switching in the knockout mice. These data suggest that CD4+ T cells that normally respond to antigens by differentiation to Th1 cells default to the Th2 pathway ...
TY - JOUR. T1 - Structural and functional abnormalities in the spleen of an mFtz-F1 gene-disrupted mouse. AU - Morohashi, Ken ichirou. AU - Tsuboi-Asai, Hisae. AU - Matsushita, Sumie. AU - Suda, Masahiro. AU - Nakashima, Manabu. AU - Sasano, Hironobu. AU - Hataba, Yoshiaki. AU - Li, Chun Li. AU - Fukata, Junichi. AU - Irie, Junji. AU - Watanabe, Takeshi. AU - Nagura, Hiroshi. AU - Li, En. PY - 1999/3/1. Y1 - 1999/3/1. N2 - The spleen has two main functions. The first is to provide a proper microenvironment to lymphoid and myeloid cells, whereas the second involves clearance of abnormal erythrocytes. Ad4BP/SF-1, a product of the mammalian FTZ-F1 gene (mFTZ-F1), was originally identified as a steroidogenic, tissue- specific transcription factor. Immunohistochemical examination of the mammalian spleens confirmed the expression of Ad4BP/SF-1 in endothelial cells of the splenic venous sinuses and pulp vein. In mFtz-F1 gene-disrupted (KO) mice, several structural abnormalities were detected in the ...
Prostate cancer is the most common type of cancer found in American men. The American Cancer Society estimates that there will be about 190,000 new cases and 27,000 deaths of prostate cancer in the United States in 2009. Genetic alterations of tumor suppressor genes are one of the most common causes of prostate cancer tumorigenesis. Our group identified Abi1Hssh3bp1 as candidate prostate tumor suppressor gene. To understand the role of Abi1Hssh3bp1 in prostate tumorigenesis we developed the conditional Abi1Hssh3bp1 KO mouse. In the first funding period we expanded our mouse colony and set up specific breeding schemes for proposed prostate tumorigenesis mouse models i.e. for prostate-specific disruption of Abi1Hssh3bp1 or simultaneous disruption of Abi1Hssh3bp1 and PTEN genes. Cre recombinase-mediated disruption of the gene was confirmed in dissected prostates of animals with Abi1Hssh3bp1 flflPbCreTg- genotype. In addition we isolated Abi1Hssh3bp1 flfl MEF cells and cloned cells lacking Abi1Hssh3bp1 to
TY - JOUR. T1 - b1-Adrenoceptors compensate for b3-adrenoceptors in ileum from b3-adrenoceptor knock-out mice. AU - Hutchinson, Dana Sabine. AU - Evans, Bronwyn A. AU - Summers, Roger J. PY - 2001. Y1 - 2001. M3 - Article. VL - 132. SP - 433. EP - 442. JO - British Journal of Pharmacology. JF - British Journal of Pharmacology. SN - 1476-5381. IS - 2. ER - ...
Aim: To determine whether high-mobility group box 1 (HMGB1) and Toll like receptor 4 (TLR4) drive the inflammatory cascade that promotes intimal hyperplasia (IH) following acute vascular injury. Methods and Results: Carotid artery wire injury in C57BL/6 mice induced a significant increase in intima to media (I/M) ratio at four weeks. Global deletion of HMGB1 using an inducible knockout mouse strain caused prevention of IH. IH was decreased by over 50% in WT mice treated with HMGB1 neutralizing antibody. Of knockout mouse strains deficient in putative receptors for HMGB1, TLR4-/- mice showed the greatest inhibition of IH. Both anti-HMGB1 treated mice and TLR4-/- mice exhibited a marked decrease in monocytic recruitment. Mice with selective depletion of TLR4 from macrophage exhibited a similar level of inhibition of IH to that seen in the global TLR4-/-. In vitro, dithiol HMGB1 dose-dependently promoted SMC migration and MCP-1/CCR2 expression, which was abolished by TLR4 inhibitory peptide. ...
TY - JOUR. T1 - Analysis of CSK homologous kinase (CHK/HYL) in hematopoiesis by utilizing gene knockout mice. AU - Hamaguchi, Isao. AU - Yamaguchi, Naoto. AU - Suda, Junko. AU - Iwama, Atsushi. AU - Hirao, Atsushi. AU - Hashiyama, Motohiro. AU - Aizawa, Shin Ichi. AU - Suda, Toshio. PY - 1996/7/5. Y1 - 1996/7/5. N2 - CHK/HYL is a non-receptor tyrosine kinase that belongs to CSK (C-terminal Src kinase) family, Northern blotting and RT-PCR analyses showed that CHK/HYL was expressed in large spectrum of hematopoietic cells except for erythroid cells and brain. To explore the function of CHK/HYL in hematopoietic cells, we generated CHK/HYL deficient mice. The mutant mice were apparently normal and fertile, while CSK knockout mice died until E11.5 from a defect in the neural tube formation. Hematological observations including blood counts and FAGS analysis showed no significant abnormalities in CHK/HYL mutant mice. CHK/HYL did not affect the activity of Src, Hck, and Fgr in cultured bone marrow ...
Is it possible to get the striatum astrocyte-specific Cre recombinase-mediated knockout of XX gene knockout mice? Any one understand how to make the knockout locate in striatum or any other good ideas to knockout one gene in one special cell from one..
TY - JOUR. T1 - PKCδ Knockout Mice Are Protected from Dextromethorphan-Induced Serotonergic Behaviors in Mice. T2 - Involvements of Downregulation of 5-HT1A Receptor and Upregulation of Nrf2-Dependent GSH Synthesis. AU - Tran, Hai Quyen. AU - Lee, Youngho. AU - Shin, Eun Joo. AU - Jang, Choon Gon. AU - Jeong, Ji Hoon. AU - Mouri, Akihiro. AU - Saito, Kuniaki. AU - Nabeshima, Toshitaka. AU - Kim, Hyoung Chun. PY - 2018/10/1. Y1 - 2018/10/1. N2 - We investigated whether a specific serotonin (5-HT) receptor-mediated mechanism was involved in dextromethorphan (DM)-induced serotonergic behaviors. We firstly observed that the activation of 5-HT1A receptor, but not 5-HT2A receptor, contributed to DM-induced serotonergic behaviors in mice. We aimed to determine whether the upregulation of 5-HT1A receptor induced by DM facilitates the specific induction of certain PKC isoform, because previous reports suggested that 5-HT1A receptor activates protein kinase C (PKC). A high dose of DM (80 mg/kg, i.p.) ...
Previous studies in male AT2R knockout mice suggest that this receptor contributes to BP control.6 Compared with their wild-type littermates, male AT2R knockout mice exhibit slightly higher systolic BP and induce a more rapid and pronounced increase in BP in secondary models of hypertension, such as volume-expansion-induced hypertension produced by deoxycorticosterone acetate-salt. Controversy exists, however, over the role of the AT2R in modulating the effectiveness of AT1R blockade at lowering BP in male rat models of renin-dependent (eg, 2-kidney, 1-clip) and -independent (eg, the spontaneously hypertensive rat) hypertension, because Ang II hypersensitivity in the absence of the AT2R may simply reflect AT1R upregulation. It is indeed a pity that female AT2R knockouts were not investigated in these studies, because one might predict that they would exhibit an even greater difference in BP and a greater degree of Ang II hypersensitivity compared with their wild-type littermates than the males, ...
Authors: Melissa M Thomas, David C Wang, Donna M DSouza, Matthew P Krause, Andrew S Layne, David S Criswell, Hayley M ONeill, Michael K Connor, Judy E Anderson, Bruce E Kemp, Gregory R Steinberg, Thomas J Hawke
The use of animal models led to great progresses in understanding the role of the endosomal adaptor Lamtor2 in endosomal/lysosomal trafficking. In a first approach LAMTOR2 knockout mice were generated, but severe defects during embryogenesis resulted in no viable offspring (Teis et al., 2006). During this time, 4 patients, all siblings, suffering from a primary immunodeficiency syndrome, due to a hypomorph LAMTOR2 allele, were identified and demanded for further investigations on the function of LAMTOR2 for the immune system (Bohn et al., 2007). Therefore, we have established conditional knockout mouse models to investigate the role of LAMTOR2 for the immune system. A special interest was put on antigen presenting cells including macrophages and dendritic cells (DCs). The correct uptake and processing of pathogens and antigen presentation in the context of the immune response is strictly regulated by the endosomal/lysosomal system. Using a mouse model where Lamtor2 was specifically depleted in ...
Experimental and clinical studies suggest that the vascular endothelium may play an important role in modulating the progression of ventricular and vascular remodeling in heart failure (HF). Impaired endothelium-dependent relaxation caused by decreased endothelial NO has been demonstrated in hypertension and HF in humans and in experimental animals.1,2⇓ NO can be produced by essentially all cell types in the heart and is known to have profound effects on cardiac function. It is synthesized from l-arginine by the catalytic reaction of 3 different isoforms of NO synthase (NOS): neuronal or type 1 NOS (nNOS), inducible or type 2 NOS (iNOS), and endothelial or type 3 NOS (eNOS). nNOS and eNOS are constitutively expressed and Ca2+-dependent enzymes, whereas iNOS is essentially expressed in macrophages and leukocytes in response to appropriate stimuli. All 3 NOS isoforms are expressed in the heart.3 NO is a potent endogenous vasodilator that is responsible for the maintenance of basal vascular tone ...
Animals. The contractile performance was studied in five young (9-14 wk of age) male TR-α1-deficient mice and five wild-type control animals of the same age and weight (28-35 g). The force-frequency relationship (see below) was studied also in muscles from four female TR-α1-deficient mice and four wild-type control mice of the same age and weight. The TR-α1-deficient mice represent a cross between the SV-129/OLa and BALB/c (30). Contractile studies were performed on four male TR-β-deficient (12) and four control mice of the same age and weight as above. This group of mice has a mixed 129/Sv and C57Bl/6J genetic background, and was generated from TR-β+/ − heterozygote backcrosses. The wild-type mice were obtained from crosses of heterozygote TR-α1- or TR-β-deficient mice. The two homozygote wild-type strains were bred in parallel with the respective knockout strains. Thus the knockout strains have the same genetic background as their respective knockout strains: 129/Ola and BALB/c for ...
The purpose of this study was to investigate the hypothesis that cardiomyocyte-specific loss of the electrogenic NBCe1 Na+-HCO3- cotransporter is cardioprotective during in vivo ischemia-reperfusion (IR) injury. An NBCe1 (Slc4a4 gene) cardiac conditional knockout mouse (KO) model was prepared by gene targeting. Cardiovascular performance of wild-type (WT) and cardiac-specific NBCe1 KO mice was analyzed by intraventricular pressure measurements, and changes in cardiac gene expression were determined by RNA Seq analysis. Response to in vivo I/R injury was analyzed after 30 minutes occlusion of the left anterior descending artery followed by 3 hours of reperfusion. Loss of NBCe1 in cardiac myocytes did not impair cardiac contractility or relaxation and caused only limited changes in gene expression patterns, such as those for electrical excitability. However, following ischemia and reperfusion, KO heart sections exhibited significantly fewer apoptotic nuclei than WT sections. These studies indicate that
The GLAST1 knockout mouse is a genetically modified mouse strain in which the gene of this member of the superfamily of the glutamate/aspartate transport proteins has been disrupted. - Italia
This work establishes an impact of cavin‐1 on pressure regulation in the pulmonary circulation. Right ventricular systolic pressure was robustly increased compared to WT littermate controls and accompanied by an increased right ventricular mass and remodeling of airway‐associated blood vessels. Because PAH is a progressive disease and we used younger animals, one may predict a more full‐blown PAH phenotype with aging. Since expression of caveolin‐1 was partly maintained, cavin‐1‐knockout mice may constitute a more adequate model of heritable PAH due to mutations in caveolin‐1 than do caveolin‐1‐knockout mice. This is because the disease‐causing mutations cause a partial reduction of caveolin‐1 (Austin et al. 2012), contrasting with the situation in caveolin‐1‐knockout mice where the protein is completely lacking.. In agreement with our current findings, thicker alveolar septa, hypercellularity, and elevated pulmonary pressure have been reported in ...
The vertebrate spinal cord is composed of billions of neurons and glia cells, which are formed in a highly coordinated manner during early neurogenesis. Specification of these cells at distinct positions along the dorsoventral (DV) axis of the developing spinal cord is controlled by a ventrally located signaling center, the medial floor plate (MFP). Currently, the origin and time frame of specification of this important organizer are not clear. During my PhD thesis, I have analyzed the function of the novel secreted growth factor Midkine-a (Mdka) in zebrafish. In higher vertebrates, mdk and the related factor pleiotrophin (ptn) are widely expressed during embryogenesis and are implicated in a variety of processes. The in-vivo function of both factors, however, is unclear, as knock-out mice show no embryonic phenotype. We have isolated two mdk co-orthologs, mdka and mdkb, and one single ptn gene in zebrafish. Molecular phylogenetic analyses have shown that these genes evolved after two large gene ...
The WT Group provides clients with a single-source engineering solution to help maintain the integrity of all projects from start to finish. With nearly 50 years of experience, WT Groups highly skilled engineering, design and consulting teams ensure consistency, clarity, and accuracy in the most cost and time-efficient manner ...
Several protein-tyrosine phosphatases (PTPs) have been proposed to act as negative regulators of insulin signaling. Recent studies have shown increased insulin sensitivity and resistance to obesity in PTP1B knockout mice, thus pointing to this enzyme as a potential drug target in diabetes. Structure-based design, guided by PTP mutants and x-ray protein crystallography, was used to optimize a relatively weak, nonphosphorus, nonpeptide general PTP inhibitor (2-(oxalyl-amino)-benzoic acid) into a highly selective PTP1B inhibitor. This was achieved by addressing residue 48 as a selectivity determining residue. By introducing a basic nitrogen in the core structure of the inhibitor, a salt bridge was formed to Asp-48 in PTP1B. In contrast, the basic nitrogen causes repulsion in other PTPs containing an asparagine in the equivalent position resulting in a remarkable selectivity for PTP1B. Importantly, this was accomplished while retaining the molecular weight of the inhibitor below 300 g/mol. ...
TY - JOUR. T1 - In vivo multiple-mouse imaging at 1.5 T. AU - Xu, S.. AU - Gade, T. P.F.. AU - Matei, C.. AU - Zakian, K.. AU - Alfieri, A. A.. AU - Hu, X.. AU - Holland, E. C.. AU - Soghomonian, S.. AU - Tjuvajev, J.. AU - Ballon, D.. AU - Koutcher, J. A.. PY - 2003/3/1. Y1 - 2003/3/1. N2 - A multiple-mouse solenoidal MR coil was developed for in vivo imaging of up to 13 mice simultaneously to screen for tumors on a 1.5 T clinical scanner. For the coil to be effective as a screening tool, it should permit acquisition of MRIs in which orthotopic tumors with diameters ,2 mm are detectable in a reasonable period of time (,1 hr magnet time) and their sizes accurately measured. Using a spin echo sequence, we demonstrated that this coil provides sufficient sensitivity for moderately high resolution images (156-176 μm in plane-resolution, 1.5 mm slice thickness). This spatial resolution permitted detection of primary brain tumors in transgenic/knockout mice and orthotopic xenografts. Brain tumor size ...
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We study the molecular alterations of human rhabdomyosarcoma and other musculo-skeletal sarcomas, to dissect the mechanisms leading to unrestricted cell growth and to the inhibition of terminal differentiation. We have also developed a transgenic/knockout mouse that spontaneously develops pelvic rhabdomyosrcomas, allowing the study of early events in the natural history of ...
Transcription regulator protein BACH2 is a protein that in humans is encoded by the BACH2 gene. It contains a BTB/POZ domain at its N-terminus which forms a disulphide-linked dimer and a bZip_Maf domain at the C-terminus. Model organisms have been used in the study of BACH2 function. A conditional knockout mouse line called Bach2tm1a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed: - In-depth immunological phenotyping - in-depth bone and cartilage phenotyping GRCh38: Ensembl release 89: ENSG00000112182 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000040270 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Sasaki S, Ito E, Toki T, Maekawa T, Kanezaki R, Umenai T, Muto A, Nagai H, Kinoshita T, Yamamoto M, Inazawa J, Taketo MM, Nakahata T, Igarashi K, Yokoyama M (Aug 2000). Cloning and expression of human B ...
I am seeking to hire an individual to conduct activities for a lab that is creating animal models of learning and memory -- generating knock-out constructs, as well as, utilizing molecular biology skills to perform Cloning, Plasmid and Phage Preparation, PCR, making cDNA Libraries, Library Screening, Southern and Northern Blot Analyses, Western Blotting. Good communication and organizational skills are a plus. A likely candidate would possess a B.S., M.S. or MD degree. I represent a leading bio-tech company with research facilities in New York and can provide excellent benefits (health insurance, dental, and vision plan, paid vacation and more). A high impact, high profile position with excellent opportunity for advancement. If you know anyone that might be interested please forward this to them or contact: Stan Saxton Voice: 609-584-8733 Ext. 218 Fax: 609-584-9575 E-Mail: sis at candseek.com ...
There is variability in the whole procedure depending largely on the strain from which the stem cells have been derived. Generally cells derived from strain 129 are used. This specific strain is not suitable for many experiments (e.g., behavioural), so it is very common to backcross the offspring to other strains. Some genomic loci have been proven very difficult to knock out. Reasons might be the presence of repetitive sequences, extensive DNA methylation, or heterochromatin. The confounding presence of neighbouring 129 genes on the knockout segment of genetic material has been dubbed the flanking-gene effect.[6] Methods and guidelines to deal with this problem have been proposed.[7][8]. Another limitation is that conventional (i.e. non-conditional) knockout mice develop in the absence of the gene being investigated. At times, loss of activity during development may mask the role of the gene in the adult state, especially if the gene is involved in numerous processes spanning development. ...
Mice have been used as models of human disease because of their physiological and genetic similarities to humans 1. Since the development of the transgenic mouse in 1982 2, numerous manipulations of the mouse genome have been created to ultimately increase the understanding of human cancer. An initial study performed by Donehower et al. 3 introduced a null mutation of the human p53 suppressor gene into a normal p53 gene using homologous recombination. This was performed in mice embryonic stem cells to determine the role of the p53 in tumorigenesis and human malignancies.. The gene encoding p53 is considered a tumor suppressor gene when it appears in its non-mutated form. However, when mutation or deletion of the gene occurs, it is thought to act as an oncogene, inducing the formation of tumors 4. Mutations and loss of the p53 gene have been linked to human tumor formations in a number of organs such as the lung, breast, colon, esophagus, liver, bladder, ovary and brain 5. Findings of p53 gene ...
When bred to mice with a Cre recombinase gene, exon 1 of the targeted gene is deleted in the |i|cre|/i| expressing tissue(s); these conditional knockout mice may be useful in generating early neural progenitor cell-specific mutants. This mutant strain may be useful in studies such as apoptosis in neural development and loss of Notch1 heterozygosity.
T cell emigration from the thymus is essential for immunological homeostasis. While stromal cell-produced sphingosine-1-phosphate (S1P) has been shown to promote thymocyte egress via the S1P receptor, S1PR1, the significance of S1P/S1PR1 signaling in the thymic stromal cells that surround T cells remains unclear. To address this issue, we developed conditional knockout mice (Lyve1-CRE/S1pr1f/f mice) in which S1pr1 was selectively targeted in cells expressing the lymphatic endothelial cell marker, Lyve1. In these mice, T cells were significantly reduced in secondary lymphoid tissues, and CD62L+ mature CD4 and CD8 single-positive (SP) T cells accumulated in the medulla failed to undergo thymus egress. Using a Lyve1 reporter strain in which Lyve1 lineage cells expressed tdTomato fluorescent protein, we unexpectedly found that a considerable proportion of the thymocytes were fluorescently labeled, indicating that they belonged to the Lyve1 lineage. The CD4 and CD8 SP thymocytes in Lyve1-CRE/S1pr1f/f mice
The researchers instead embarked on creating Cre-loxP conditional knock out mice for Ezh2. The technique involves two transgenic mouse strains, one carries Cre, an enzyme, under the control of a B or T cell promoter gene. The other strain, in this case, carries the Ezh2 gene surrounded by a special binding site called loxP. LoxP sites on DNA are recognizable by the Cre enzyme. When Cre mice are bred with mice carrying the loxP surrounded Ezh2 gene, the resulting mice lack Ezh2 gene only in developing B cells. As a result the Ezh2 needed in embryonic development is not deterred in these mice. This in vivo model of studying cell signaling is invaluable ...
SRC-2 coactivator deficiency decreases functional reserve in response to pressure overload of mouse heart.s profile, publications, research topics, and co-authors
CompoZr Zinc Finger Nuclease (ZFN) Technology is a novel system for rapid creation of targeted gene knockouts, genomic insertions or gene editing in eukaryotic systems. ZFNs are highly efficient pairs of custom nucleases designed and made by Sigma-Aldrich to target your gene or genomic sequence of interest. ZFNs (mRNA or plasmid formats) are delivered to cells by transfection methods or to embryos by microinjection. Upon cleavage of the target site, endogenous cellular processes are harnessed to produce targeted mutations that result in gene knockout.
DISC1 mutant mice exhibit greater responses to an NMDA antagonist, MK-801, and D-serine treatment[a] Locomotor activity in open field of male mice before and af
Increased Anxiety-Like Behavior and Enhanced Synaptic Efficacy in the Amygdala of GluR5 Knockout Mice. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
TY - JOUR. T1 - IL-4, IL-10 and IFNγ production in TGFβ1-null mice fed low doses of OVA. AU - Barone, K. S.. AU - Tolarova, D.. AU - Ormsby, I.. AU - Doetschman, T.. AU - Michael, J. G.. PY - 1998/3/20. Y1 - 1998/3/20. N2 - Previous studies by others have indicated that feeding low doses of antigen induces active suppression, mediated by the release of inhibitory cytokines, particularly TGFβ1. However, we have recently shown that low dose oral tolerance can be generated in the absence of TGFβ1 using TGFβ1 null mutant mice. In the present study, the level of IL-4, IL-10 and IFNγ was examined in cell supernatants of TGFβ1 null mutant mice fed low doses of OVA. Neonates identified as either control (+/+ or +/-) or TGFβ1-null (-/-) mice were given injections of anti-CD11α (anti-LFA-1) every other day from day 2 after birth until weaning. Anti-CD11α has previously been shown to extend the life of TGFβ1-null mice. Mice were then gavaged with either water or 1 mg of OVA for three days. Eight ...
Background The human 9p21. crazy type. We observed considerable, tissue-specific compensatory rules of the and genes among the various knockout mice, making the effects on atherosclerosis hard to interpret. Conclusions takes on a protective part against atherosclerosis, whereas appears to be modestly proatherogenic. However, no connection was found between the 9p21 genotype and the transcription of 9p21 neighboring genes in main human being aortic vascular cells in vitro. There is considerable compensatory rules in the highly conserved 9p21 orthologous region in mice. and gene were found to have improved atherosclerotic lesions in an ApoE null background GW-786034 with significant attenuation of apoptosis in lesions as well as with cultured main macrophages and vascular clean muscle mass GW-786034 cells.17 However, to day no observation regarding atherosclerotic phenotype has been made involving the additional neighboring genes. We set out to survey the 9p21.3 orthologous region using knockout ...
UNG KO cell line available now. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon 1 and Insertion of the selection cassette in exon 1.
HMIC KO cell line available now. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 3 and 28 bp deletion in exon 3.