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Results for “Gene knockout”

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At least 145 records · Page 8Linked to original sources

PubMed1999

Microglial reaction in some CNS nuclei following nerves transection in BALB/c and interferon-gamma gene knockout mice.

The present study was aimed to ascertain if the endogenous IFN-gamma is necessary for induction of microglial reaction associated with the CNS neurons after neurectomy of the vagus and hypoglossal nerves in IFN-gamma gene knockout mice and BALB/c mice serving as controls. Vigorous microglial reaction as detected by Mac-1 antibody was elicited in the brainstem nuclei in both strains of mice. Increased Mac-1 immunoreactivity in microglia was detected as early as 1 day post-operation in the ipsilateral dorsal nucleus of vagus, nucleus ambiguus and the hypoglossal nucleus; a similar feature was observed in the nucleus tractus solitarius bilaterally. Mac-1 immunoreactivity in reactive microglia appeared to increase with survival intervals and was comparable throughout in both strains of mice. It is therefore concluded that endogenous IFN-gamma is not responsible for upregulation of complement type 3 receptor immunomolecules in reactive microglia following nerves sectioning.

Animals↗

PubMed2005

Compensatory response of IL-1 gene knockout mice after pulmonary infection with Klebsiella pneumoniae.

This study was designed to determine the role of interleukin (IL)-1 in the inflammatory response against experimentally induced pneumonia caused by Klebsiella pneumoniae. The host immune responses of IL-1 gene knockout (IL-1 KO) mice and immunocompetent wild-type (WT) mice were compared after pulmonary infection with K. pneumoniae. There were no significant differences between the survival rates and viable bacterial counts in lungs and blood of IL-1 KO and WT mice after pulmonary infections under different conditions. Histopathological analysis showed a similar inflammatory response in both groups of mice. However, in the early stage of infection, the level of tumour necrosis factor alpha (TNF-alpha) in homogenized lungs of IL-1 KO mice was significantly higher than in WT mice. To determine the role of endogenous TNF-alpha in the recovery of the defence mechanism in IL-1 KO mice, mice were treated with an anti-TNF-alpha mAb before infection with K. pneumoniae. The results revealed a significantly lower survival rate of anti-TNF-alpha mAb-treated IL-1 KO mice than BSA-treated IL-1 KO mice. The data suggest that compensatory production of TNF-alpha in IL-1 KO mice contributes to the host defence against K. pneumoniae infection.

Animals↗

PubMed2001

Characterization of glycosylphosphatidylinositol-anchored decay accelerating factor (GPI-DAF) and transmembrane DAF gene expression in wild-type and GPI-DAF gene knockout mice using polyclonal and monoclonal antibodies with dual or single specificity.

Decay-accelerating factor (DAF, CD55) is a glycosylphosphatidylinositol (GPI)-linked membrane inhibitor of complement activation. While human and other mammalian species contain only one DAF gene, two distinct DAF genes, referred to as GPI-DAF and transmembrane (TM)-DAF, respectively, have been identified in the mouse. Using several independently generated monoclonal and polyclonal antibodies, either with dual or single specificity for GPI-DAF and TM-DAF gene products, we have examined the expression of the two DAF genes in tissues of the wild-type and a strain of knockout mouse whose GPI-DAF gene has been inactivated. By fluorescence-activated cell sorting (FACS) analysis, we found that DAF protein is present on the wild-type mouse erythrocytes and lymphocytes but no signal was detectable on the same cells of GPI-DAF gene knockout mice. Both T and B lymphocytes and splenic macrophages express the GPI-DAF gene but the expression level is higher on B lymphocytes than on T lymphocytes. Within the T cell population, both CD4+ and CD8+ T cells are positive. DAF protein was detected by immunohistochemistry at high levels on wild-type mouse spermatids and mature sperm. In contrast, only mature sperm stained positive in the GPI-DAF gene knockout mouse testis, suggesting that GPI-DAF but not the TM-DAF gene is expressed on spermatids. Examination of the fetoplacental unit at the day 7.5 stage revealed that GPI-DAF but not the TM-DAF gene is expressed in the maternal decidua cells surrounding the trophoectoderm of the embryo. No DAF expression was detected on trophoblast or the embryo proper. These findings suggest that although the TM-DAF gene is irrelevant on mouse blood cells, the two DAF genes may have different roles in germ cell development and/or mature sperm function. Because complement receptor 1-related gene/protein y (Crry) has been shown to be expressed on early mouse embryos, the complete lack of GPI-DAF and TM-DAF gene expression in early mouse development may explain the observed sensitivity of Crry-deficient embryos to maternal complement attack.

Animals↗

PubMed2001

Targeted gene knockout of inner arm 1 in Tetrahymena thermophila.

Cilia and flagella contain at least eight different types of dynein arms. It is not entirely clear how the different types of arms are organized along the axoneme. In addition, the role each different type of dynein plays in ciliary or flagellar motility is not known. To initiate studies of dynein organization and function in cilia, we have introduced a mutation into one dynein heavy chain gene (DYH6) in Tetrahymena themophila by targeted gene knockout. We have generated mutant cells that lack wild-type copies of the DYH6 gene. We have shown that the DYH6 gene encodes one heavy chain (HC2) of Tetrahymena 18S dynein and that 18S dynein occupies the I1 position in the ciliary axoneme. We have also shown that Tetrahymena I1 is required for normal motility, normal feeding and normal doubling rate.

Amino Acid Sequence↗

PubMed2005

Expression of endothelial nitric oxide synthase is suppressed in the renal vasculature of angiotensinogen-gene knockout mice.

We have attempted to elucidate the mechanism by which endothelial-type nitric oxide synthase (eNOS) is regulated in the kidney, with special reference to the role of renal hemodynamics and angiotensin II (Ang II). We compared angiotensinogen gene knockout (Atg-/-) mice, which lacked Ang II (resulting in sodium/water depletion and severe hypotension), with wild-type (Atg+/+) mice. Using Western blot analysis and the NADPH diaphorase histochemical reaction, we found that the expression and activity of eNOS were markedly lower in the renal vessels of Atg-/- mice compared with wild-type (Atg+/+) mice. Dietary salt loading significantly enhanced renal eNOS levels and increased blood pressure in Atg-/- mice, but severe hypotension almost abolished the effects of salt loading. In contrast, in Atg+/+ mice, altered salt intake or hydralazine had no effect on renal eNOS levels. These results suggest that perfusion pressure plays an essential role in maintaining renal vascular eNOS activity, whereas Ang II plays a supportive role, especially when renal circulation is impaired.

Angiotensin II↗

PubMed1995

Accelerated clearance of Onchocerca microfilariae and resistance to reinfection in interleukin-4 gene knockout mice.

Immunity to Onchocerca microfilariae (mf) in mice is associated with CD4+ Th2 cells and is dependent on IL-5. In view of the role of IL-4 in the development of Th2 cells, we have utilized IL-4 gene knockout mice (IL-4-/-) to investigate microfilarial clearance and resistance to reinfection. Paradoxically, in the absence of IL-4 there is accelerated clearance of microfilariae during a primary infection and unimpeded expression of resistance to reinfection. IL-4-/- mice showed a lack of an IgE response although peripheral eosinophilia was equivalent to wildtype controls. The data presented here suggest that elimination of mf can occur independent of IL-4 and that in this model it may even be detrimental to the host.

Animals↗

PubMed2005

Expression of cyclooxygenase-2 in the juxtaglomerular apparatus of angiotensinogen gene-knockout mice.

AIMS: The present study was designed to examine the role of the renin-angiotensin system in the regulation of macula densa cyclooxygenase-2 (COX-2) during altered dietary salt intake. METHODS: We investigated COX-2 expression in the macula densa of angiotensinogen gene-knockout (Atg-/-) mice. COX-2 expression in the renal cortex was determined by real-time quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. RESULTS: The renal cortical expression of COX-2 mRNA increased 24.7 times in Atg-/- mice compared with Atg+/+ mice. When Atg-/- mice were fed a high-salt diet (4% NaCl) for 10 days, the levels of COX-2 expression were markedly suppressed. The macula densa COX-2 immunoreactivity was correlated with the mRNA expression. The selective inhibition of neuronal isoform of nitric oxide synthase (N-NOS) activity by 7-nitroindazole significantly reduced the levels of COX-2 mRNA in Atg-/- mice by 54.1%. CONCLUSION: These results suggest that (1) COX-2 activity in the macula densa can be regulated by salt intake through a mechanism independent of the renin-angiotensin system, and (2) COX-2 expression is functionally linked to renal cortical N-NOS activity in Atg-/- mice.

Angiotensinogen↗

PubMed2003

Angiotensinogen gene knockout delays and attenuates cold-induced hypertension.

The aim of the present study was to assess our hypothesis that the renin-angiotensin system (RAS) is responsible for cold-induced hypertension and cardiac hypertrophy. Two groups of wild-type (WT) mice and 2 groups of angiotensinogen gene knockout (Agt-KO) mice (6 per group) were used. After blood pressures (BP) of the four groups were measured 3 times at room temperature (25 degrees C), 1 WT and 1 Agt-KO group were exposed to cold (5 degrees C). The remaining groups were kept at 25 degrees C. BP of the cold-exposed WT group increased significantly in 1 week of cold exposure and rose gradually to 168+/-7 mm Hg by week 5, whereas the BP of the Agt-KO group did not increase until week 3. The cold-induced increase in BP (DeltaBP) was decreased significantly in the Agt-KO mice (19+/-3 mm Hg) compared with that of the WT mice (61+/-5 mm Hg) by 5 weeks of exposure to cold. Both WT and Agt-KO groups had cardiac hypertrophy in cold to the same extent. Agt-KO caused a significant increase in nitric oxide (NO) production. Thus, the RAS may inhibit NO formation. Chronic cold exposure decreased NO production, which may be mediated partially by activation of the RAS. These results strongly support that the RAS plays a critical role in the development of cold-induced hypertension but not cardiac hypertrophy. Moreover, the role of the RAS in cold-induced hypertension may be mediated in part by its inhibition on NO production. The findings also reveal the possible relation between the RAS and NO in cardiovascular regulation.

Angiotensinogen↗

PubMed2004

Vasopressin stimulates ventromedial hypothalamic neurons via oxytocin receptors in oxytocin gene knockout male and female mice.

A wealth of neuropharmacological data demonstrates that oxytocin (OT) actions in the mammalian forebrain support a wide variety of affiliative behaviors and repress aggressive behaviors. Based on that literature, it was expected that reproductive and affiliative behaviors would be vastly decreased and aggression markedly increased in OT gene knockout (OTKO) mice. The initial publications reporting the behaviors of these mice did not include such phenotypes. Here, we compared single-unit activities recorded from the ventromedial hypothalamus in tissue slices of male and female OTKO mice and their wild-type littermate to test two hypotheses about OT functional genomics. First, we proposed that in OTKO mice, a very similar 9-amino-acid neuropeptide, arginine vasopressin (a likely gene duplication product), can 'cross over' and compensate for the lack of OT. This hypothesis was confirmed in both males and females. Further, we proposed that because of the lifelong absence of OT in OTKO, OT receptors would be more sensitive to OT in the knockout animals. We tested this idea in males and found that it was correct. Thus, an answer to the 'OTKO paradox' is put forth, with implications for OT-sensitive behaviors in a variety of species.

Animals↗

PubMed2004

The construction of gene knockouts in the cyanobacterium Synechocystis sp. PCC 6803.

A series of protocols are presented for the storage, growth, transformation, and characterization of wild-type (wt) and mutant strains of Synechocystis PCC 6803. These protocols include the isolation of genomic DNA and the strategies required for the construction of specific gene knockouts in this organism. This cyanobacterium has been used widely as a model for photosynthesis research and the sequence of its genome, together with a database of mutants that have already been constructed, is available at CyanoBase (http://kazusa.or.jp/cyano/). The details provided in this chapter do not assume any previous experience in working with cyanobacteria and are intended to enable new investigators to take advantage of a wide-range of gene modification and mutation mapping techniques that have been adapted for use in this system.

Cyanobacteria↗

PubMed2002

Anxiety-related behaviors in cholecystokinin-A, B, and AB receptor gene knockout mice in the plus-maze.

Cholecystokinin (CCK)-A receptor (AR) and B receptor (BR) share highly amino acid sequence homology and overlap in their tissue distribution. We examined the anxiety-related behavior of CCK-AR, CCK-BR, and CCK-ARBR gene knockout (-/-) mice in the elevated plus-maze. CCK-AR(-/-) mice showed a significantly higher frequency of open-arm entries than wild-type and CCK-BR(-/-) mice, whereas the percentage open-arm entry values in CCK-AR(-/-) mice did not differ from those in wild-type mice. Thus, this increased frequency in open-arm entries for CCK-AR(-/-) mice was interpreted to be due to an increase in locomotor activity, rather than to a reduction in anxiety. By contrast, CCK-BR(-/-) mice showed significantly lower percentage open-arm entry values and spent significantly less time in the open- arms than wild-type and CCK-AR(-/-) mice. We therefore conclude that a lack of CCK-BR increases the anxiety-related behavior of the mouse in the elevated plus- maze.

Analysis of Variance↗

PubMed2000

Inducible nitric oxide synthase gene knockout mice have increased resistance to gut injury and bacterial translocation after an intestinal ischemia-reperfusion injury.

OBJECTIVE: Intestinal ischemia-reperfusion after severe shock states is often associated with bacterial translocation and intestinal barrier dysfunction. Our previous studies showed that inducible nitric oxide synthase (iNOS) gene knockout mice were resistant to endotoxin-induced bacterial translocation and ileal mucosal damage. The goal of this study was to test whether iNOS mediates bacterial translocation after intestinal ischemia-reperfusion, using iNOS knockout mice (iNOS-/-) and their wild-type littermates (iNOS+/+). DESIGN: Prospective animal study with concurrent controls. SETTING: Small animal laboratory. SUBJECTS: Thirty-eight iNOS knockout mice and 51 wild-type littermates. INTERVENTIONS: iNOS+/+ mice or iNOS-/- mice were subjected to a sham operation or 30 mins of superior mesenteric artery occlusion followed by reperfusion. Twenty-four hours after reperfusion, bacterial translocation to mesenteric lymph nodes, ileal villous damage, and cecal bacterial population were evaluated. MEASUREMENTS AND MAIN RESULTS: Sham operation did not induce bacterial translocation, change cecal bacterial population levels, or cause ileal villous damage. Intestinal ischemia-reperfusion caused bacterial translocation in 72% of the iNOS+/+ mice but only 28% of the iNOS-/- mice. Both iNOS+/+ and iNOS-/- mice subjected to superior mesenteric artery occlusion (SMAO) in which bacterial translocation occurred had cecal bacterial population levels that were three logs higher than mice subjected to sham SMAO or mice subjected to SMAO in which bacterial translocation did not occur. The magnitude of villous injury was less in the iNOS-/- mice than the iNOS+/+ mice after SMAO, although the incidence of ileal villous damage was significantly higher in both the iNOS+/+ and iNOS-/- mice in which bacterial translocation occurred after SMAO than in the mice in which bacterial translocation did not occur after SMAO. iNOS+/+ mice subjected to SMAO had increased plasma concentrations of nitrite (NO2-) and nitrate (NO3-), and the plasma concentrations of NO2- and NO3- were highest in the mice in which bacterial translocation had occurred. CONCLUSION: iNOS knockout mice were more resistant to intestinal ischemia-reperfusion-induced bacterial translocation and mucosal injury than wild-type mice, suggesting that iNOS might play a role in intestinal ischemia-reperfusion-induced loss of gut barrier function.

Animals↗

PubMed1998

Murine graft-versus-host disease in an F1-hybrid model using IFN-gamma gene knockout donors.

These experiments were performed to determine whether the absence of donor-derived IFN-gamma would influence the outcome of acute graft-vs-host disease (GVHD). Graft-vs-host reactions were induced in B6D2F1 hybrids using grafts from either IFN-gamma gene knockout (gko) or wild-type, C57BL/6J, parental strain donors. GVHD was equally lethal in both groups, but IFN-gamma gko graft recipients developed a more protracted form of the disease. These mice developed early wasting that persisted until death. IFN-gamma was present in spleen cell cultures from wild-type graft recipients, but was absent in cultures from IFN-gamma gko graft recipients. Both recipient groups showed macrophage priming for LPS-induced TNF-alpha release. Engraftment of donor-derived CD4+ and CD8+ cells was greater in IFN-gamma gko graft recipients. Pathologic changes in IFN-gamma gko graft recipients were different from those typically seen in acute GVHD. The syndrome developing in IFN-gamma gko recipients consisted of patchy alopecia, corneal dryness and clouding, and lymphocytic infiltration of the liver, pancreas, salivary gland, lung, and kidney. Lymphocytic infiltrates were also present in the epidermis and the epithelium of both bile and salivary gland ducts. Some of the lesions closely resembled those seen in the "sicca"/Sjogren's-like syndrome associated with chronic GVHD; however, there was no evidence of immune complex deposition in the kidney. These results indicate that GVHD in IFN-gamma gko graft recipients shares many features with acute GVHD, but both the duration of the disease and its pathologic manifestations are different. Our results suggest that IFN-gamma plays a significant role in the pathogenesis of acute GVHD by increasing the rate at which mortality develops.

Animals↗

PubMed2003

Role of gene knockout and transgenic mice in the study of xenobiotic metabolism.

The role of P450s in xenobiotic metabolism, toxicity, and carcinogenicity has been studied for many years by using in vitro approaches and limited in vivo investigations. Genetic analysis to study the effects of xenobiotics in intact animals has only recently been carried out by use of gene knockout mice. Mice lacking expression of these enzymes have no or only modest phenotypes, indicating that their xenobiotic-metabolizing enzymes are not critical for mammalian development or physiological homeostasis. The null mice have been used to study the roll of xenobiotic-metabolizing enzymes in chemical toxicity and carcinogenicity. There are marked species differences in the expression and catalytic activities of P450s that metabolize xenobiotics, and this complicates the extrapolation of data obtained in rodents for use in drug development and human risk assessment. This is especially notable between mice and rats, commonly used experimental models, and humans. To begin to develop more predictive models, P450 humanized mice were produced and characterized by using genomic clones containing the complete coding and regulatory regions of genes, as transgenes. Humanized lines expressing CYP2D6 and CYP3A4 human P450 were characterized and found to accurately express human P450 proteins and catalytic activities at levels comparable to or higher than the corresponding activities found in human tissues. These novel mouse lines offer the opportunity to predict human drug and carcinogen metabolism and disposition and to search for endogenous substrates for human P450s.

Animals↗

PubMed2004

Dual role of tumor necrosis factor-alpha in hepatic ischemia-reperfusion injury: studies in tumor necrosis factor-alpha gene knockout mice.

Although hepatic ischemia-reperfusion (IR) injury is partially mediated by tumor necrosis factor-alpha (TNF), we recently found that low-dose TNF before IR is hepatoprotective. We examined the seemingly conflicting roles of TNF in mediating liver injury in a partial hepatic IR model using TNF gene knockout (TNF ko) mice to allow TNF replacement at specified times. Compared with wild-type mice, TNF ko mice exhibit minimal alanine aminotransferase release and few hepatonecrotic lesions during the early (time, 2 hours) and late (time, 24 hours) phases of IR. TNF ko mice differed from wild-type mice in that TNF ko mice exhibited no activation or induction of nuclear factor-kappa B, p38, cyclin D1, or proliferating cell nuclear antigen after IR. A single low-dose TNF injection 1 minute before the onset of hepatic ischemia restored hepatic IR injury in TNF ko mice. To clarify the importance of TNF for hepatoprotection, preconditioning (10 minutes of ischemia and 10 minutes of reperfusion) was performed before the onset of IR for TNF ko mice whose capacity to undergo IR injury had been restored by TNF replacement. Ischemic preconditioning failed to protect these mice from TNF-augmented IR injury; however, following the administration of intravenous TNF (1 microg per kg body weight, which mimics the early increase in hepatic and plasma TNF levels that is mobilized by ischemic preconditioning), significant hepatoprotection against both the early and late phases of TNF-augmented IR injury was observed. In conclusion, TNF appears to mediate both the early and late phases of liver injury in hepatic IR, but it also is an essential mediator of hepatoprotective effects brought about by ischemic preconditioning.

Animals↗

PubMed2001

Caspase-3 gene knockout defines cell lineage specificity for programmed cell death signaling in the ovary.

Previous studies have proposed the involvement of caspase-3, a downstream executioner enzyme common to many paradigms of programmed cell death (PCD), in mediating the apoptosis of both germ and somatic cells in the ovary. Herein we used caspase-3 gene knockout mice to directly test for the functional requirement of this protease in oocyte and/or granulosa cell demise. Using both in vivo and in vitro approaches, we determined that oocyte death initiated as a result of either developmental cues or pathological insults was unaffected by the absence of caspase-3. However, granulosa cells of degenerating antral follicles in both mouse and human ovaries showed a strong immunoreaction using an antibody raised against the cleaved (activated) form of caspase-3. Furthermore, caspase-3 mutant female mice possessed aberrant atretic follicles containing granulosa cells that failed to be eliminated by apoptosis, as confirmed by TUNEL (terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling) analysis of DNA cleavage and 4',6-diamidino-2-phenylindole staining of nuclear morphology (pyknosis). These in vivo results were supported by findings from in vitro cultures of wild-type and caspase-3-deficient antral follicles or isolated granulosa cells. Contrasting the serum starvation-induced occurrence of apoptosis in wild-type granulosa cells, caspase-3-null granulosa cells deprived of hormonal support were TUNEL-negative, showed attenuated chromatin condensation by 4',6-diamidino-2-phenylindole staining and exhibited delayed internucleosomal DNA cleavage. Such ex vivo findings underscore the existence of a cell autonomous (granulosa cell intrinsic) defect in apoptosis execution resulting from caspase-3 deficiency. We conclude that caspase-3 is functionally required for granulosa cell apoptosis during follicular atresia, but that the enzyme is dispensable for germ cell apoptosis in the female.

Animals↗

PubMed2003

Metabolic flux analysis of pykF gene knockout Escherichia coli based on 13C-labeling experiments together with measurements of enzyme activities and intracellular metabolite concentrations.

Metabolic flux analysis based on 13C-labeling experiments followed by the measurement of intracellular isotope distribution using both 2D NMR and GC-MS was carried out to investigate the effect of pyruvate kinase (pyk) gene knockout on the metabolism of Escherichia coli in continuous culture. In addition, the activities of 16 enzymes, and the concentrations of 5 intracellular metabolites, were measured as a function of time in batch culture as well as continuous culture. It was found that flux through phosphoenol pyruvate carboxylase and malic enzyme were up-regulated in the pykF- mutant as compared with the wild type, and acetate formation was significantly reduced in the mutant. In addition, flux through the phosphofructose kinase pathway was reduced and that through the oxidative pentose phosphate (PP) pathway increased in the mutant. This was evidenced by the corresponding enzyme activities, and the increase in the concentrations of phosphoenol pyruvate, glucose-6-phosphate and 6-phosphogluconate, etc. It was also found for continuous cultivation that the enzyme activities of the oxidative PP and Entner-Doudoroff pathways increased as the dilution rate increased for the pykF- mutant. To clarify the metabolism quantitatively, it was found to be quite important to integrate the information on intracellular metabolic flux distribution, enzyme activities and intracellular metabolite concentrations.

Acetic Acid↗

PubMed2006

Tissue distribution of basigin and monocarboxylate transporter 1 in the adult male mouse: a study using the wild-type and basigin gene knockout mice.

Basigin (Bsg) is a transmembrane protein that is responsible for targeting of monocarboxylate transporters (MCTs) to the cell membrane. The present study was conducted to determine whether or not Bsg was required for the proper localization of MCT isoform 1 (MCT1) in a wide range of tissues in adult male mice. The tissue distributions of Bsg and MCT1 in wild-type (WT) mice, the tissue distribution of MCT1 in Bsg gene knockout (Bsg-KO) mice, and the protein and mRNA levels of MCT1 in both genotypes were studied. Immunohistochemistry demonstrated that Bsg colocalized with MCT1 in the cerebrum, retina, skeletal and cardiac muscle, duodenal epithelium, hepatic sinusoid, proximal uriniferous tubules, Leydig cells, and efferent ductule epithelium in WT mice. Bsg was absent but MCT1 was present in Sertoli cells, cauda epididymis, myoepithelial cells and duct of the mandibular gland, surface epithelium of the stomach and bronchioles. In Bsg-KO mice, with the exception of Leydig cells, MCT1 immunostaining was greatly reduced in intensity and its distribution was altered in tissues that expressed both Bsg and MCT1 in WT mice. Levels of the protein and mRNA for MCT1 in these tissues did not change significantly in Bsg-KO mice. On the other hand, immunostaining patterns in cells in which Bsg was absent but MCT1 was present in WT mice remained unchanged in Bsg-KO mice. These observations suggest that Bsg is required for the proper localization of MCT1 in a wide range of cells but not in every cell type.

Animals↗