Relevant bibliographies by topics / Lp82 / Journal articles

Journal articles on the topic 'Lp82'

To see the other types of publications on this topic, follow the link: Lp82.
Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Lp82.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Ma, H., M. Shih, I. Hata, C. Fukiage, M. Azuma, and T. R. Shearer. "Lp85 calpain is an enzymatically active rodent-specific isozyme of lens Lp82." Current Eye Research 20, no. 3 (January 2000): 183–89. http://dx.doi.org/10.1076/0271-3683(200003)2031-9ft183.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Fukiage, Chiho, Emi Nakajima, Hong Ma, Mitsuyoshi Azuma, and Thomas R. Shearer. "Characterization and Regulation of Lens-specific Calpain Lp82." Journal of Biological Chemistry 277, no. 23 (March 19, 2002): 20678–85. http://dx.doi.org/10.1074/jbc.m200697200.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Shearer, T. R., H. Ma, M. Shih, I. Hata, C. Fukiage, Y. Nakamura, and M. Azuma. "Lp82 calpain during rat lens maturation and cataract formation." Current Eye Research 17, no. 11 (January 1998): 1037–43. http://dx.doi.org/10.1076/ceyr.17.11.1037.5232.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

NAKAMURA, Y., C. FUKIAGE, H. MA, M. SHIH, M. AZUMA, and T. R. SHEARER. "Decreased Sensitivity of Lens-Specific Calpain Lp82 to Calpastatin Inhibitor." Experimental Eye Research 69, no. 2 (August 1999): 155–62. http://dx.doi.org/10.1006/exer.1998.0686.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

MA, H., I. HATA, M. SHIH, C. FUKIAGE, Y. NAKAMURA, M. AZUMA, and T. R. SHEARER. "Lp82 is the Dominant Form of Calpain in Young Mouse Lens." Experimental Eye Research 68, no. 4 (April 1999): 447–56. http://dx.doi.org/10.1006/exer.1998.0625.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ueda, Yoji, Ashley L. McCormack, Thomas R. Shearer, and Larry L. David. "Purification and Characterization of Lens Specific Calpain (Lp82) from Bovine Lens." Experimental Eye Research 73, no. 5 (November 2001): 625–37. http://dx.doi.org/10.1006/exer.2001.1071.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Gao, Junyuan, Xiurong Sun, Francisco J. Martinez-Wittinghan, Xiaohua Gong, Thomas W. White, and Richard T. Mathias. "Connections Between Connexins, Calcium, and Cataracts in the Lens." Journal of General Physiology 124, no. 4 (September 27, 2004): 289–300. http://dx.doi.org/10.1085/jgp.200409121.

Full text
Abstract:
There is a good deal of evidence that the lens generates an internal micro circulatory system, which brings metabolites, like glucose, and antioxidants, like ascorbate, into the lens along the extracellular spaces between cells. Calcium also ought to be carried into the lens by this system. If so, the only path for Ca2+ to get out of the lens is to move down its electrochemical gradient into fiber cells, and then move by electrodiffusion from cell to cell through gap junctions to surface cells, where Ca-ATPase activity and Na/Ca exchange can transport it back into the aqueous or vitreous humors. The purpose of the present study was to test this calcium circulation hypothesis by studying calcium homeostasis in connexin (Cx46) knockout and (Cx46 for Cx50) knockin mouse lenses, which have different degrees of gap junction coupling. To measure intracellular calcium, FURA2 was injected into fiber cells, and the gradient in calcium concentration from center to surface was mapped in each type of lens. In wild-type lenses the coupling conductance of the mature fibers was ∼0.5 S/cm2 of cell to cell contact, and the best fit to the calcium concentration data varied from 700 nM in the center to 300 nM at the surface. In the knockin lenses, the coupling conductance was ∼1.0 S/cm2 and calcium varied from ∼500 nM at the center to 300 nM at the surface. Thus, when the coupling conductance doubled, the concentration gradient halved, as predicted by the model. In knockout lenses, the coupling conductance was zero, hence the efflux path was knocked out and calcium accumulated to ∼2 μM in central fibers. Knockout lenses also had a dense central cataract that extended from the center to about half the radius. Others have previously shown that this cataract involves activation of a calcium-dependent protease, Lp82. We can now expand on this finding to provide a hypothesis on each step that leads to cataract formation: knockout of Cx46 causes loss of coupling of mature fiber cells; the efflux path for calcium is therefore blocked; calcium accumulates in the central cells; at concentrations above ∼1 μM (from the center to about half way out of a 3-wk-old lens) Lp82 is activated; Lp82 cleaves cytoplasmic proteins (crystallins) in central cells; and the cleaved proteins aggregate and scatter light.
APA, Harvard, Vancouver, ISO, and other styles
8

MA, H., M. SHIH, I. HATA, C. FUKIAGE, M. AZUMA, and T. R. SHEARER. "Protein for Lp82 Calpain Is Expressed and Enzymatically Active in Young Rat Lens." Experimental Eye Research 67, no. 2 (August 1998): 221–29. http://dx.doi.org/10.1006/exer.1998.0515.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Inomata, Mitsushi, Masami Hayashi, Yoshimasa Ito, Yuko Matsubara, Makoto Takehana, Seiichi Kawashima, and Seigo Shumiya. "Comparison of Lp82- and m-calpain-mediated proteolysis during cataractogenesis in Shumiya cataract rat (SCR)." Current Eye Research 25, no. 4 (January 2002): 207–13. http://dx.doi.org/10.1076/ceyr.25.4.207.13486.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Azuma, Mitsuyoshi, Yoshiyuki Tamada, Sayaka Kanaami, Emi Nakajima, Yoshikuni Nakamura, Chiho Fukiage, Neil E. Forsberg, Melinda K. Duncan, and Thomas R. Shearer. "Differential influence of proteolysis by calpain 2 and Lp82 on in vitro precipitation of mouse lens crystallins." Biochemical and Biophysical Research Communications 307, no. 3 (August 2003): 558–63. http://dx.doi.org/10.1016/s0006-291x(03)01194-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

Ueda, Yoji, Chiho Fukiage, Marjorie Shih, Thomas R. Shearer, and Larry L. David. "Mass Measurements of C-terminally Truncated α-Crystallins from Two-dimensional Gels Identify Lp82 as a Major Endopeptidase in Rat Lens." Molecular & Cellular Proteomics 1, no. 5 (May 2002): 357–65. http://dx.doi.org/10.1074/mcp.m200007-mcp200.

Full text
APA, Harvard, Vancouver, ISO, and other styles
12

Li, H. Y., H. Osman, C. W. Kang, T. Ba, and J. Lou. "Numerical and experimental studies of water disinfection in UV reactors." Water Science and Technology 80, no. 8 (October 15, 2019): 1456–65. http://dx.doi.org/10.2166/wst.2019.394.

Full text
Abstract:
Abstract Performance of UV reactors for water disinfection is investigated in this paper. Both experimental and numerical studies are performed on base reactor LP24. Enterobacteria phage MS2 is chosen as the challenge microorganism in the experiments. Experiments are conducted to evaluate the effect of different parameters, i.e. flow rate and UV transmission, on the reactor performance. Simulation is carried out based on the commercial software ANSYS FLUENT with user defined functions (UDFs) implemented. The UDF is programmed to calculate UV dose absorbed by different microorganisms along their flow trajectories. The effect with boundary layer mesh and without boundary layer mesh for LP24 is studied. The results show that the inclusion of boundary layer mesh does not have much effect on the reactor performance in terms of reduction equivalent dose (RED). The numerical results agree well with the experimental measurements, hence validating the numerical model. With this achieved, the numerical model is applied to study other scaled reactors: LP12, LP40, LP60 and LP80. Comparisons show that LP40 has the highest RED and log inactivation among all the reactors while LP80 has the lowest RED and log inactivation.
APA, Harvard, Vancouver, ISO, and other styles
13

Späth, Gerald F., Lon-Fye Lye, Hiroaki Segawa, Salvatore J. Turco, and Stephen M. Beverley. "Identification of a Compensatory Mutant (lpg2−REV) of Leishmania major Able To Survive as Amastigotes within Macrophages without LPG2-Dependent Glycoconjugates and Its Significance to Virulence and Immunization Strategies." Infection and Immunity 72, no. 6 (June 2004): 3622–27. http://dx.doi.org/10.1128/iai.72.6.3622-3627.2004.

Full text
Abstract:
ABSTRACT Different Leishmania species rely to different extents on abundant glycoconjugates, such as lipophosphoglycan (LPG) and related molecules, in mammalian infections. Previously, we showed that Leishmania major deletion mutants lacking the Golgi GDP-mannose transporter LPG2, which is required for assembly of the dominant phosphoglycan (PG) repeats of LPG, were unable to survive in macrophages. These lpg2 − mutants, however, retained the ability to generate asymptomatic, persistent infections in mice. In contrast, Ilg and colleagues showed that Leishmania mexicana LPG2 mutants retained virulence for mice. Here we identified a partial revertant population of the L. major lpg2 − mutants (designated lpg2 − REV) that had regained the ability to replicate in macrophages and induce disease pathology through a compensatory change. Like the lpg2 parent, the lpg2 − REV revertant was unable to synthesize LPG2-dependent PGs in the promastigote stage and thus remained highly attenuated in the ability to induce infection. However, after considerable delay lpg2 − REV revertant-infected mice exhibited lesions, and amastigotes isolated from these lesions were able to replicate within macrophages despite the fact that they were unable to synthesize PGs. Thus, in some respects, the lpg2 − REV amastigotes resemble L. mexicana amastigotes. Future studies of the gene(s) responsible may shed light on the mechanisms employed by L. major to survive in the absence of LPG2-dependent glycoconjugates and may also improve the potential of the lpg2 − L. major line to serve as a live parasite vaccine by overcoming its tendency to revert toward virulence.
APA, Harvard, Vancouver, ISO, and other styles
14

Yun, C. Chris, Hong Sun, Dongsheng Wang, Raluca Rusovici, Amanda Castleberry, Randy A. Hall, and Hyunsuk Shim. "LPA2 receptor mediates mitogenic signals in human colon cancer cells." American Journal of Physiology-Cell Physiology 289, no. 1 (July 2005): C2—C11. http://dx.doi.org/10.1152/ajpcell.00610.2004.

Full text
Abstract:
Lysophosphatidic acid (LPA) is a mediator of multiple cellular responses. LPA mediates its effects predominantly through the G protein-coupled receptors LPA1, LPA2, and LPA3. In the present work, we studied LPA2-mediated signaling using human colon cancer cell lines, which predominantly express LPA2. LPA2 activated Akt and Erk1/2 in response to LPA. LPA mediated Akt activation was inhibited by pertussis toxin (PTX), whereas Erk1/2 activation was completely inhibited by a blocker of phospholipase Cβ, U-73122. LPA also induced interleukin-8 (IL-8) synthesis in the colon cancer cells by primarily activating LPA2 receptor. We also found that LPA2 interacts with Na+/H+ exchanger regulatory factor 2 (NHERF2). Activation of Akt and Erk1/2 was significantly attenuated by silencing of NHERF2 expression by RNA interference, suggesting a pivotal role of NHERF2 in LPA2-mediated signaling. We found that expression of LPA2 was elevated, whereas expression of LPA1 downregulated in several types of cancers, including ovarian and colon cancer. We conclude that LPA2 is the major LPA receptor in colon cancer cells and cellular signals by LPA2 are largely mediated through its ability to interact with NHERF2.
APA, Harvard, Vancouver, ISO, and other styles
15

Dulebohn, Daniel P., Aaron Bestor, and Patricia A. Rosa. "Borrelia burgdorferi Linear Plasmid 28-3 Confers a Selective Advantage in an Experimental Mouse-Tick Infection Model." Infection and Immunity 81, no. 8 (June 10, 2013): 2986–96. http://dx.doi.org/10.1128/iai.00219-13.

Full text
Abstract:
ABSTRACTBorrelia burgdorferi, the bacterium that causes Lyme disease, has a unique segmented genome consisting of numerous linear and circular plasmids and a linear chromosome. Many of these genetic elements have been found to encode factors critical forB. burgdorferito complete the infectious cycle. However, several plasmids remain poorly characterized, and their roles during infection withB. burgdorferihave not been elucidated. To more fully characterize the role of one of the four 28-kb linear plasmids, lp28-3, we generated strains specifically lacking lp28-3 and assayed the contribution of genes carried by lp28-3 toB. burgdorferiinfection. We found that lp28-3 does not carry any genes that are strictly required for infection of a mouse or tick and that lp28-3-deficient spirochetes are competent at causing a disseminated infection. Interestingly, spirochetes containing lp28-3 were at a selective advantage compared to lp28-3-deficient spirochetes when coinjected into a mouse, and this advantage was reflected in the population of spirochetes acquired by feeding ticks. Our data demonstrate that genes carried by lp28-3, although not essential, contribute to the fitness ofB. burgdorferiduring infection.
APA, Harvard, Vancouver, ISO, and other styles
16

Labandeira-Rey, Maria, and Jonathan T. Skare. "Decreased Infectivity in Borrelia burgdorferi Strain B31 Is Associated with Loss of Linear Plasmid 25 or 28-1." Infection and Immunity 69, no. 1 (January 1, 2001): 446–55. http://dx.doi.org/10.1128/iai.69.1.446-455.2001.

Full text
Abstract:
ABSTRACT Previous reports indicated a correlation between loss of plasmids and decreased infectivity of Borrelia burgdorferi strain B31, suggesting that plasmids may encode proteins that are required for pathogenesis. In this study, we expand on this correlation. Using theB. burgdorferi genomic sequence, we designed primers specific for each plasmid, and by using PCR we catalogued 11 linear and 2 circular plasmids from 49 clonal isolates of a mid-passage B. burgdorferi strain B31, initially derived from infected mouse skin, and 20 clones obtained from mouse skin infected with a low-passage isolate of B. burgdorferi strain B31. Among the 69 clones analyzed, nine distinct genotypes were identified relative to wild-type B. burgdorferi strain B31. Among the nine clonal genotypes obtained, only the 9-kb circular plasmid (cp9), the 25-kb linear plasmid (lp25), and either the 28-kb linear plasmid 1 or 4 (lp28-1 and lp28-4, respectively) were missing, in different combinations. We compared the infectivity of the wild-type strain, containing all known B. burgdorferi plasmids, with those of single mutants lacking either lp28-1, lp28-4, or lp25 and a double mutant missing both cp9 and lp28-1. The infectivity data indicated thatB. burgdorferi strain B31 cells lacking lp28-4 were modestly attenuated in all tissues analyzed, whereas samples missing lp25 were completely attenuated in all tissues, even at the highest inoculum tested. Isolates without lp28-1 infected the joint tissue yet were not able to infect other tissues as effectively. In addition, we have observed a selection in vivo in the skin, bladder, and joint for cells containing lp25 and in the skin and bladder for cells containing lp28-1, indicating that lp25 and lp28-1 encode proteins required for colonization and short-term maintenance in these mammalian tissues. In contrast, there was no selection in the joint for cells containing lp28-1, suggesting that genes on lp28-1 are not required for colonization of B. burgdorferi within the joint. These observations imply that the dynamic nature of the B. burgdorferi genome may provide the genetic heterogeneity necessary for survival in the diverse milieus that this pathogen occupies in nature and may contribute to tropism in certain mammalian host tissues.
APA, Harvard, Vancouver, ISO, and other styles
17

Oh, Yong-Seok, Nam Won Jo, Jung Woong Choi, Hyeon Soo Kim, Sang-Won Seo, Kyung-Ok Kang, Jong-Ik Hwang, et al. "NHERF2 Specifically Interacts with LPA2 Receptor and Defines the Specificity and Efficiency of Receptor-Mediated Phospholipase C-β3 Activation." Molecular and Cellular Biology 24, no. 11 (June 1, 2004): 5069–79. http://dx.doi.org/10.1128/mcb.24.11.5069-5079.2004.

Full text
Abstract:
ABSTRACT Lysophosphatidic acid (LPA) activates a family of cognate G protein-coupled receptors and is involved in various pathophysiological processes. However, it is not clearly understood how these LPA receptors are specifically coupled to their downstream signaling molecules. This study found that LPA2, but not the other LPA receptor isoforms, specifically interacts with Na+/H+ exchanger regulatory factor2 (NHERF2). In addition, the interaction between them requires the C-terminal PDZ domain-binding motif of LPA2 and the second PDZ domain of NHERF2. Moreover, the stable expression of NHERF2 potentiated LPA-induced phospholipase C-β (PLC-β) activation, which was markedly attenuated by either a mutation in the PDZ-binding motif of LPA2 or by the gene silencing of NHERF2. Using its second PDZ domain, NHERF2 was found to indirectly link LPA2 to PLC-β3 to form a complex, and the other PLC-β isozymes were not included in the protein complex. Consistently, LPA2-mediated PLC-β activation was specifically inhibited by the gene silencing of PLC-β3. In addition, NHERF2 increases LPA-induced ERK activation, which is followed by cyclooxygenase-2 induction via a PLC-dependent pathway. Overall, the results suggest that a ternary complex composed of LPA2, NHERF2, and PLC-β3 may play a key role in the LPA2-mediated PLC-β signaling pathway.
APA, Harvard, Vancouver, ISO, and other styles
18

Contos, James J. A., Isao Ishii, Nobuyuki Fukushima, Marcy A. Kingsbury, Xiaoqin Ye, Shuji Kawamura, Joan Heller Brown, and Jerold Chun. "Characterization of lpa2 (Edg4) and lpa1/lpa2 (Edg2/Edg4) Lysophosphatidic Acid Receptor Knockout Mice: Signaling Deficits without Obvious Phenotypic Abnormality Attributable to lpa2." Molecular and Cellular Biology 22, no. 19 (October 1, 2002): 6921–29. http://dx.doi.org/10.1128/mcb.22.19.6921-6929.2002.

Full text
Abstract:
ABSTRACT Lysophosphatidic acid (LPA), a bioactive lipid produced by several cell types including postmitotic neurons and activated platelets, is thought to be involved in various biological processes, including brain development. Three cognate G protein-coupled receptors encoded by lpa1 /lp A1/Edg-2/Gpcr26, lpa2 /lp A2/Edg-4, and lpa3 /lp A3/Edg-7 mediate the cellular effects of LPA. We have previously shown that deletion of lpa1 in mice results in craniofacial dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of pups with frontal hematoma. To further investigate the role of these receptors and LPA signaling in the organism, we deleted lpa2 in mice. Homozygous knockout (lpa2 (−/−)) mice were born at the expected frequency and displayed no obvious phenotypic abnormalities. Intercrosses allowed generation of lpa1 (−/−) lpa2 (−/−) double knockout mice, which displayed no additional phenotypic abnormalities relative to lpa1 (−/−) mice except for an increased incidence of perinatal frontal hematoma. Histological analyses of lpa1 (−/−) lpa2 (−/−) embryonic cerebral cortices did not reveal obvious differences in the proliferating cell population. However, many LPA-induced responses, including phospholipase C activation, Ca2+ mobilization, adenylyl cyclase activation, proliferation, JNK activation, Akt activation, and stress fiber formation, were absent or severely reduced in embryonic fibroblasts derived from lpa1 (−/−) lpa2 (−/−) mice. Except for adenylyl cyclase activation [which was nearly abolished in lpa1 (−/−) fibroblasts], these responses were only partially affected in lpa1 (−/−) and lpa2 (−/−) fibroblasts. Thus, although LPA2 is not essential for normal mouse development, it does act redundantly with LPA1 to mediate most LPA responses in fibroblasts.
APA, Harvard, Vancouver, ISO, and other styles
19

Labandeira-Rey, Maria, J. Seshu, and Jonathan T. Skare. "The Absence of Linear Plasmid 25 or 28-1 of Borrelia burgdorferi Dramatically Alters the Kinetics of Experimental Infection via Distinct Mechanisms." Infection and Immunity 71, no. 8 (August 2003): 4608–13. http://dx.doi.org/10.1128/iai.71.8.4608-4613.2003.

Full text
Abstract:
ABSTRACT The 25-kb linear plasmid lp25 and one of the 28-kb linear plasmids (lp28-1) are required for experimental infection in Borrelia burgdorferi, the etiologic agent of Lyme disease. The loss of these plasmids either eliminates infectivity (lp25) or significantly increases the 50% infective dose during a 2-week infection period (lp28-1). This study assessed the kinetics of bacterial dissemination in C3H/HeN mice infected with B. burgdorferi lacking either lp25 or lp28-1, as well as their wild-type parent, and tracked the development of specific borrelial antibodies over a 3-week period. The results indicated that the wild type and the lp28-1− strains were able to disseminate throughout the host, whereas the lp25− strain was cleared within 48 h of inoculation. While the wild-type B. burgdorferi persisted in tissues for the duration of the study, the lp28-1− mutant began clearing at day 8, with no detectable bacteria present by day 18. As expected, the wild-type strain persisted in C3H/HeN mice despite a strong humoral response; however, the lp28-1− mutant was cleared coincidently with the development of a modest immunoglobulin M response. The lp28-1− mutant was able to disseminate and persist in C3H-scid mice at a level indistinguishable from that of wild-type cells, confirming that acquired immunity was required for clearance in C3H/HeN mice. Thus, within an immunocompetent host, lp28-1-encoded proteins are not required for dissemination but are essential for persistence associated with Lyme borreliosis.
APA, Harvard, Vancouver, ISO, and other styles
20

Ab Ghani, Rosmida Binti, Najah Binti Mohd Nawi, and Norhafiza Binti Idris. "Levels Politechnic Community Satisfaction to The Use of Lebuhraya Pantai Timur 2." Jurnal Konseling dan Pendidikan 6, no. 3 (November 30, 2018): 121. http://dx.doi.org/10.29210/128000.

Full text
Abstract:
Construction of East Coast Expressway 2 (LPT2) has a large impact in being able to link the states on the East Coast in a time shorter than existing roads. This gives a more comfortable alternative ride to the local community and beyond. However, there are still complaints from users regarding the facilities and services provided in LPT2. Thus, a study carried out to determine the level of satisfaction of polytechnic communities against the use of LPT2. A total of 222 respondent from four polytechnic involved in this study. Analysis of the findings made by using descriptive statistic and T-test through the software Statistical Package for Social Science (SPSS) version 23. Results of this analysis showed a mean value for items 'security level' in LPT2 is 2.29, i.e. at low mean score. While the 'facilities provided' is 2.50, where the stage score mean intermediate. Analysis of T-test also found, there is no significant relationship between the levels of satisfaction of users of different gender. Pearson correlation analysis found that the relationship between the usage frequency of LPT2 and the user satisfaction level was weak, but significant. It is hoped that the findings could help provides an overview of the level of satisfaction of the security aspects of polytechnic communities and facilities in LPT2. This can help the parties responsible for providing the best service to oversee and improve LPT2 in all aspects in order to provide optimum satisfaction to the user.
APA, Harvard, Vancouver, ISO, and other styles
21

Embers, Monica E., Xavier Alvarez, Tara Ooms, and Mario T. Philipp. "The Failure of Immune Response Evasion by Linear Plasmid 28-1-Deficient Borrelia burgdorferi Is Attributable to Persistent Expression of an Outer Surface Protein." Infection and Immunity 76, no. 9 (July 14, 2008): 3984–91. http://dx.doi.org/10.1128/iai.00387-08.

Full text
Abstract:
ABSTRACT Infectivity and persistence by Borrelia burgdorferi, the etiologic agent of Lyme disease, rely stringently on regulatory events. Among these is the downregulation of lipoprotein antigen expression, exemplified by outer surface protein C (OspC), at the advent of specific immunity in the mammalian host. B. burgdorferi spirochetes that lack the linear plasmid 28-1 (lp28-1) succumb to the host's immune response. We thus explored the notion that these two phenomena were related—that lp28-1− organisms fail to downregulate ospC and thus are cleared following the appearance of anti-OspC antibody in the murine host. The lp-28-1− isolate and a wild-type (wt) isolate bearing the complete set of plasmids were grown in dialysis membrane chambers that were implanted into rat peritoneal cavities. Analysis of mRNA and protein from these cultures showed that OspC expression levels by lp28-1− organisms are abnormally high in vivo. A time course analysis of ospC expression in tissues following infection indicates also that temporal diminution of the dominant antigen OspC is impaired in lp28-1− spirochetes. Finally, passive transfer of monoclonal OspC-specific antibody into SCID mice 8 days postinfection cleared lp28-1− spirochetes, yet the wt organisms persisted in a majority of animals. These findings indicate that incomplete repression of OspC by lp28-1− organisms renders them susceptible to immune-mediated clearance. The lp28-1 plasmid must harbor one or more genes involved in OspC downregulation.
APA, Harvard, Vancouver, ISO, and other styles
22

Chen, Min, L. Nicole Towers, and Kathleen L. O'Connor. "LPA2 (EDG4) mediates Rho-dependent chemotaxis with lower efficacy than LPA1 (EDG2) in breast carcinoma cells." American Journal of Physiology-Cell Physiology 292, no. 5 (May 2007): C1927—C1933. http://dx.doi.org/10.1152/ajpcell.00400.2006.

Full text
Abstract:
Lysophosphatidic acid (LPA) acts via binding to specific G protein-coupled receptors and has been implicated in the biology of breast cancer. Here, we characterize LPA receptor expression patterns in common established breast cancer cell lines and their contribution to breast cancer cell motility. By measuring expression of the LPA receptors LPA1, LPA2, and LPA3 with real-time quantitative PCR, we show that the breast cancer cell lines tested can be clustered into three main groups: cells that predominantly express LPA1 (BT-549, Hs578T, MDA-MB-157, MDA-MB-231, and T47D), cells that predominantly express LPA2 (BT-20, MCF-7, MDA-MB-453, and MDA-MB-468), and a third group that shows comparable expression level of these two receptors (MDA-MB-175 and MDA-MB-435). LPA3 expression was detected primarily in MDA-MB-157 cells. Using a Transwell chemotaxis assay to monitor dose response, we find that cells predominantly expressing LPA1 have a peak migration rate at 100 nM LPA that drops off dramatically at 1 μM LPA, whereas cells predominantly expressing LPA2 show the peak migration rate at 1 μM LPA, which remains high at 10 μM. Using BT-20 cells, LPA2-specific small interfering RNA, and C3 exotransferase, we demonstrate that LPA2 can mediate LPA-stimulated cell migration and activation of the small GTPase RhoA. Using LPA2 small interfering RNA, exogenous expression of LPA1, and treatment with Ki16425 LPA receptor antagonist in the BT-20 cells, we further find that LPA1 and LPA2 cooperate to promote LPA-stimulated chemotaxis. In summary, our results suggest that the expression of both LPA1 and LPA2 may contribute to chemotaxis and may permit cells to respond optimally to a wider range of LPA concentrations, thus revealing a new aspect of LPA signaling.
APA, Harvard, Vancouver, ISO, and other styles
23

Lawrenz, Matthew B., R. Mark Wooten, and Steven J. Norris. "Effects of vlsE Complementation on the Infectivity of Borrelia burgdorferi Lacking the Linear Plasmid lp28-1." Infection and Immunity 72, no. 11 (November 2004): 6577–85. http://dx.doi.org/10.1128/iai.72.11.6577-6585.2004.

Full text
Abstract:
ABSTRACT The loss of linear plasmid lp28-1, which contains the vls antigenic variation locus, is associated with reduced infectivity of Borrelia burgdorferi in immunocompetent mice. The recombinant shuttle vector pBBE22, which includes the virulence determinant BBE22 from lp25 and restores infectivity to readily transformable B. burgdorferi lacking lp25 and lp56, was used to determine the effect of trans expression of vlsE on virulence. Spirochetes lacking lp28-1 were complemented with the plasmid pBBE22:vlsE, containing both BBE22 and vlsE. VlsE protein produced by this construct was expressed and surface accessible in in vitro-cultured B. burgdorferi, as determined by surface proteolysis and immunoblot analysis. Clones lacking lp25 but containing lp28-1 and either pBBE22 or pBBE22:vlsE were reisolated consistently from immunocompetent mice 8 weeks after infection. In contrast, a clone lacking both lp25 and lp28-1 and complemented with pBBE22:vlsE was isolated from only a single tissue of one of six C3H/HeN mice 8 weeks postinfection. These results indicate that either an intact vls antigenic variation locus or another determinant on lp28-1 is required to restore complete infectivity. In addition, an isogenic clone that retained lp28-1 was complemented with the vlsE shuttle plasmid and was examined for vlsE sequence variation and infectivity. Sequence variation was not observed for the shuttle plasmid, indicating that the cis arrangement of vlsE and the vls silent cassettes in lp28-1 facilitate vlsE gene conversion. Lack of vlsE sequence variation on the shuttle plasmid thus did not result in clearance of the trans-complemented strain in immunocompetent mice under the conditions tested.
APA, Harvard, Vancouver, ISO, and other styles
24

Rinaldi, Mariana Roennau Lemos, Eduardo Martinelli de Lima, Luciane Macedo de Menezes, Susana Maria Deon Rizzatto, Paulo Ricardo Baccarin Matje, and Roberto Vanin Pinto Ribeiro. "Eruption rates of lower second premolars at different development stages evaluated with cone-beam computed tomography." Angle Orthodontist 87, no. 4 (September 29, 2016): 570–75. http://dx.doi.org/10.2319/071116-548.1.

Full text
Abstract:
ABSTRACT Objective: To evaluate and compare the eruption rates of lower second premolars (LPm2) at different developmental stages using cone-beam computed tomography (CBCT). Materials and Methods: Retrospectively, 31 individuals (9.77 ± 1.25 years) had their LPm2 scored according to the Demirjian method, and afterwards they were split into three groups according to developmental stage, as follows: D = complete-formed crowns; E = root length less than crown height; and F = root length greater than or equal to crown height. Linear distances from the LPm2 crown tip to the anatomical reference line (ARL) and to the occlusal plane line (OPL) were measured in paired CBCT scans (T1, T2), taken with an average interval of 8.6 months between them. Eruption rates (mm/y) were calculated and then compared between groups. Results: Eruption rates were greater for LPm2 at stage F than at stages D or E (P < .01) regardless of whether they were measured from the ARL (D = 2.84 mm/y; E = 2.55 mm/y; F = 5.38 mm/y) or from the OPL (D = 1.82 mm/y; E = 2.02 mm/y; F = 5.26 mm/y). Eruption rates evaluated from the ARL and the OPL had no statistically significant differences (P = .052), and a positive correlation (r = .79, P < .001) between them was observed. Conclusions: LPm2 at Demirjian stage F showed greater eruption rates than at stages D or E, regardless of whether rates were measured from the ARL or the OPL. Faster eruption is expected for LPm2 at stage F. Evaluation of the LPm2's developmental stage using CBCT can aid in clinical decision making regarding the correct timing for intervention.
APA, Harvard, Vancouver, ISO, and other styles
25

Long, Jaclyn, Peter Darroch, Kah Fei Wan, Kok Choi Kong, Nicholas Ktistakis, Nigel J. Pyne, and Susan Pyne. "Regulation of cell survival by lipid phosphate phosphatases involves the modulation of intracellular phosphatidic acid and sphingosine 1-phosphate pools." Biochemical Journal 391, no. 1 (September 26, 2005): 25–32. http://dx.doi.org/10.1042/bj20050342.

Full text
Abstract:
We have shown previously that LPPs (lipid phosphate phosphatases) reduce the stimulation of the p42/p44 MAPK (p42/p44 mitogen-activated protein kinase) pathway by the GPCR (G-protein-coupled receptor) agonists S1P (sphingosine 1-phosphate) and LPA (lysophosphatidic acid) in serum-deprived HEK-293 cells [Alderton, Darroch, Sambi, McKie, Ahmed, N. J. Pyne and S. Pyne (2001) J. Biol. Chem. 276, 13452–13460]. In the present study, we now show that this can be blocked by pretreating HEK-293 cells with the caspase 3/7 inhibitor, Ac-DEVD-CHO [N-acetyl-Asp-Glu-Val-Asp-CHO (aldehyde)]. Therefore LPP2 and LPP3 appear to regulate the apoptotic status of serum-deprived HEK-293 cells. This was supported further by: (i) caspase 3/7-catalysed cleavage of PARP [poly(ADP-ribose) polymerase] was increased in serum-deprived LPP2-overexpressing compared with vector-transfected HEK-293 cells; and (ii) serum-deprived LPP2- and LPP3-overexpressing cells exhibited limited intranucleosomal DNA laddering, which was absent in vector-transfected cells. Moreover, LPP2 reduced basal intracellular phosphatidic acid levels, whereas LPP3 decreased intracellular S1P in serum-deprived HEK-293 cells. LPP2 and LPP3 are constitutively co-localized with SK1 (sphingosine kinase 1) in cytoplasmic vesicles in HEK-293 cells. Moreover, LPP2 but not LPP3 prevents SK1 from being recruited to a perinuclear compartment upon induction of PLD1 (phospholipase D1) in CHO (Chinese-hamster ovary) cells. Taken together, these data are consistent with an important role for LPP2 and LPP3 in regulating an intracellular pool of PA and S1P respectively, that may govern the apoptotic status of the cell upon serum deprivation.
APA, Harvard, Vancouver, ISO, and other styles
26

Lin, Songbai, Sei-Jung Lee, Hyunsuk Shim, Jerold Chun, and C. Chris Yun. "The absence of LPA receptor 2 reduces the tumorigenesis by ApcMin mutation in the intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 5 (November 2010): G1128—G1138. http://dx.doi.org/10.1152/ajpgi.00321.2010.

Full text
Abstract:
Lysophosphatidic acid (LPA) is a lipid mediator that mediates several effects that promote cancer progress. The LPA receptor type 2 (LPA2) expression is often elevated in several types of cancers, including colorectal cancer (CRC). In this study, we investigated the role of LPA2 in the development of intestinal adenomas by comparing Apc Min/+ mice with Apc Min/+ /Lpar2 −/− mice. There were 50% fewer intestinal adenomas in Apc Min/+ /Lpar2 −/− mice than Apc Min/+ mice. Smaller-size adenomas (<1 mm) were found at higher frequencies in Apc Min/+ /Lpar2 −/− mice compared with Apc Min/+ mice at the two age groups examined. The expression level of LPA2 correlated with increased size of intestinal adenomas. Reduced tumor multiplicity and size in Apc Min/+ /Lpar2 −/− mice correlated with decreased proliferation of intestinal epithelial cells. Apc Min/+ /Lpar2 −/− mice showed an increased level of apoptosis, suggesting that LPA2-mediated signaling stimulates intestinal tumor development and progress by regulating both cell proliferation and survival. In addition, the expression levels of Krüpple-like factor 5 (KLF5), β-catenin, cyclin D1, c-Myc, and hypoxia-inducible factor-1α (HIF-1α) were significantly altered in Apc Min/+ /Lpar2 −/− mice compared with Apc Min/+ mice. In vitro studies using HCT116 cells showed that LPA induced cyclin D1, c-Myc, and HIF-1α expression, which was attenuated by knockdown of LPA2. In summary, intestinal tumor initiated by Apc mutations is altered by LPA2-mediated signaling, which regulates tumor growth and survival by altering multiple targets.
APA, Harvard, Vancouver, ISO, and other styles
27

Liu, Dong, Chahnaz Kebaier, Nazzy Pakpour, Althea A. Capul, Stephen M. Beverley, Phillip Scott, and Jude E. Uzonna. "Leishmania major Phosphoglycans Influence the Host Early Immune Response by Modulating Dendritic Cell Functions." Infection and Immunity 77, no. 8 (June 1, 2009): 3272–83. http://dx.doi.org/10.1128/iai.01447-08.

Full text
Abstract:
ABSTRACT The precise role of Leishmania glycoconjugate molecules including phosphoglycans (PGs) and lipophosphoglycan (LPG) on host cellular responses is still poorly defined. Here, we investigated the interaction of Leishmania major LPG2 null mutant (lpg2 − ), which lacks both PGs and LPG, with dendritic cells (DCs) and the subsequent early immune response in infected mice. Surprisingly, the absence of phosphoglycans did not influence expression pattern of major histocompatibility complex class II (MHC II), CD40, CD80, and CD86 on DCs in vitro and in vivo. However, lpg2 − L. major induced significantly higher production of interleukin-12p40 (IL-12p40) by infected bone marrow-derived DCs (BMDCs) than wild-type (WT) parasites in vitro. Furthermore, the production of IL-12p40 by draining lymph node cells from lpg2 − mutant-infected mice was higher than those from WT L. major-infected mice. In model antigen presentation experiments, DCs from lpg2 − mutant-infected mice induced more gamma interferon (IFN-γ) and IL-2 production by Leishmania-specific T cells than those from WT-infected mice. Lymphocytes isolated from mice infected for 3 days with lpg2 − parasites produce similar levels of IFN-γ, but significantly less IL-4 and IL-10 than WT controls. Decreased IL-4 production was also seen in another general PG-deficient mutant lacking the Golgi UDP-galactose transporters (lpg5A − lpg5B − ), but not with the lpg1 − mutant lacking only LPG, thereby implicating PGs generally in the reduction of IL-4 production. Thus, Leishmania PGs influence host early immune response by modulating DC functions in a way that inhibits antigen presentation and promotes early IL-4 response, and their absence may impact the balance between Th1 and Th2 responses.
APA, Harvard, Vancouver, ISO, and other styles
28

Geng, Hui, Rongpei Lan, Yaguang Liu, Wei Chen, Meng Wu, Pothana Saikumar, Joel M. Weinberg, and Manjeri A. Venkatachalam. "Proximal tubule LPA1 and LPA2 receptors use divergent signaling pathways to additively increase profibrotic cytokine secretion." American Journal of Physiology-Renal Physiology 320, no. 3 (March 1, 2021): F359—F374. http://dx.doi.org/10.1152/ajprenal.00494.2020.

Full text
Abstract:
Lysophosphatidic acid (LPA) increases platelet-derived growth factor-B (PDGFB) and connective tissue growth factor (CTGF) production and secretion by proximal tubule (PT) cells through LPA2 receptor-Gqα-αvβ6-integrin-mediated activation of transforming growth factor-β1 (TGFB1). LPA2, β6-integrin, PDGFB, and CTGF increase in kidneys after ischemia-reperfusion injury (IRI), coinciding with fibrosis. The TGFB1 receptor antagonist SD-208 prevents increases of β6-integrin, TGFB1-SMAD signaling, and PDGFB/CTGF expression after IRI and ameliorates fibrosis (Geng H, Lan R, Singha PK, Gilchrist A, Weinreb PH, Violette SM, Weinberg JM, Saikumar P, Venkatachalam MA. Am J Pathol 181: 1236‐1249, 2012; Geng H, Lan R, Wang G, Siddiqi AR, Naski MC, Brooks AI, Barnes JL, Saikumar P, Weinberg JM, Venkatachalam MA. Am J Pathol 174: 1291‐1308, 2009). We report now that LPA1 receptor signaling through epidermal growth factor receptor (EGFR)-ERK1/2-activator protein-1 cooperates with LPA2-dependent TGFB1 signaling to additively increase PDGFB/CTGF production and secretion by PT cells. Conversely, inhibition of both pathways results in greater suppression of PDGFB/CTGF production and secretion and promotes greater PT cellular differentiation than inhibiting one pathway alone. Antagonism of the LPA-generating enzyme autotaxin suppressed signaling through both pathways. After IRI, kidneys showed not only more LPA2, nuclear SMAD2/3, and PDGFB/CTGF but also increased LPA1 and autotaxin proteins, together with enhanced EGFR/ERK1/2 activation. Remarkably, the TGFB1 receptor antagonist SD-208 prevented all of these abnormalities excepting increased LPA2. SD-208 inhibits only one arm of LPA signaling: LPA2-Gqα-αvβ6-integrin-dependent production of active TGFB1 and its receptor-bound downstream effects. Consequently, far-reaching protection by SD-208 against IRI-induced signaling alterations and tubule-interstitial pathology is not fully explained by our data. TGFB1-dependent feedforward modulation of LPA1 signaling is one possibility. SD-208 effects may also involve mitigation of injury caused by IRI-induced TGFB1 signaling in endothelial cells and monocytes. Our results have translational implications for using TGFB1 receptor antagonists, LPA1 and LPA2 inhibitors concurrently, and autotaxin inhibitors in acute kidney injury to prevent the development of chronic kidney disease.
APA, Harvard, Vancouver, ISO, and other styles
29

Zhang, Weiqiang, Himabindu Penmatsa, Aixia Ren, Chandanamali Punchihewa, Andrew Lemoff, Bing Yan, Naoaki Fujii, and Anjaparavanda P. Naren. "Functional regulation of cystic fibrosis transmembrane conductance regulator-containing macromolecular complexes: a small-molecule inhibitor approach." Biochemical Journal 435, no. 2 (March 29, 2011): 451–62. http://dx.doi.org/10.1042/bj20101725.

Full text
Abstract:
CFTR (cystic fibrosis transmembrane conductance regulator) has been shown to form multiple protein macromolecular complexes with its interacting partners at discrete subcellular microdomains to modulate trafficking, transport and signalling in cells. Targeting protein–protein interactions within these macromolecular complexes would affect the expression or function of the CFTR channel. We specifically targeted the PDZ domain-based LPA2 (type 2 lysophosphatidic acid receptor)–NHERF2 (Na+/H+ exchanger regulatory factor-2) interaction within the CFTR–NHERF2–LPA2-containing macromolecular complexes in airway epithelia and tested its regulatory role on CFTR channel function. We identified a cell-permeable small-molecule compound that preferentially inhibits the LPA2–NHERF2 interaction. We show that this compound can disrupt the LPA2–NHERF2 interaction in cells and thus compromises the integrity of macromolecular complexes. Functionally, it elevates cAMP levels in proximity to CFTR and upregulates its channel activity. The results of the present study demonstrate that CFTR Cl− channel function can be finely tuned by modulating PDZ domain-based protein–protein interactions within the CFTR-containing macromolecular complexes. The present study might help to identify novel therapeutic targets to treat diseases associated with dysfunctional CFTR Cl− channels.
APA, Harvard, Vancouver, ISO, and other styles
30

Li, Chunying, Keanna S. Dandridge, Anke Di, Kevin L. Marrs, Erica L. Harris, Koushik Roy, John S. Jackson, et al. "Lysophosphatidic acid inhibits cholera toxin-induced secretory diarrhea through CFTR-dependent protein interactions." Journal of Experimental Medicine 202, no. 7 (October 3, 2005): 975–86. http://dx.doi.org/10.1084/jem.20050421.

Full text
Abstract:
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated chloride channel localized primarily at the apical or luminal surfaces of epithelial cells that line the airway, gut, and exocrine glands; it is well established that CFTR plays a pivotal role in cholera toxin (CTX)-induced secretory diarrhea. Lysophosphatidic acid (LPA), a naturally occurring phospholipid present in blood and foods, has been reported to play a vital role in a variety of conditions involving gastrointestinal wound repair, apoptosis, inflammatory bowel disease, and diarrhea. Here we show, for the first time, that type 2 LPA receptors (LPA2) are expressed at the apical surface of intestinal epithelial cells, where they form a macromolecular complex with Na+/H+ exchanger regulatory factor–2 and CFTR through a PSD95/Dlg/ZO-1–based interaction. LPA inhibited CFTR-dependent iodide efflux through LPA2-mediated Gi pathway, and LPA inhibited CFTR-mediated short-circuit currents in a compartmentalized fashion. CFTR-dependent intestinal fluid secretion induced by CTX in mice was reduced substantially by LPA administration; disruption of this complex using a cell-permeant LPA2-specific peptide reversed LPA2-mediated inhibition. Thus, LPA-rich foods may represent an alternative method of treating certain forms of diarrhea.
APA, Harvard, Vancouver, ISO, and other styles
31

Jones, M. L., C. Martoni, H. Chen, W. Ouyang, T. Metz, and S. Prakash. "Deconjugation of Bile Acids with Immobilized Genetically EngineeredLactobacillus plantarum80(pCBH1)." Applied Bionics and Biomechanics 2, no. 1 (2005): 31–38. http://dx.doi.org/10.1155/2005/380659.

Full text
Abstract:
Bile acids are important to normal human physiology. However, bile acids can be toxic when produced in pathologically high concentrations in hepatobileary and other diseases. This study shows that immobilized genetically engineeredLactobacillus plantarum80 (pCBH1) (LP80 (pCBH1)) can efficiently hydrolyze bile acids and establishes a basis for their use. Results show that immobilized LP80 (pCBH1) is able to effectively break down the conjugated bile acids into glycodeoxycholic acid (GDCA) and taurodeoxycholic acid (TDCA) with bile salt hydrolase (BSH) activities of 0.17 and 0.07 μmol DCA/mg CDW/h, respectively. The deconjugation product, deoxycholic acid (DCA), was diminished by LP80 (pCBH1) within 4 h of initial BSH activity. Thisin-vitrostudy suggests that immobilized genetically engineered bacterial cells have important potential for deconjugation of bile acids for lowering of high levels of bile acids for therapy.
APA, Harvard, Vancouver, ISO, and other styles
32

Capul, Althea A., Suzanne Hickerson, Tamara Barron, Salvatore J. Turco, and Stephen M. Beverley. "Comparisons of Mutants Lacking the Golgi UDP-Galactose or GDP-Mannose Transporters Establish that Phosphoglycans Are Important for Promastigote but Not Amastigote Virulence in Leishmania major." Infection and Immunity 75, no. 9 (July 2, 2007): 4629–37. http://dx.doi.org/10.1128/iai.00735-07.

Full text
Abstract:
ABSTRACT Abundant surface Leishmania phosphoglycans (PGs) containing [Gal(β1,4)Man(α1-PO4)]-derived repeating units are important at several points in the infectious cycle of this protozoan parasite. PG synthesis requires transport of activated nucleotide-sugar precursors from the cytoplasm to the Golgi apparatus. Correspondingly, null mutants of the L. major GDP-mannose transporter LPG2 lack PGs and are severely compromised in macrophage survival and induction of acute pathology in susceptible mice, yet they are able to persist indefinitely and induce protective immunity. However, lpg2 − L. mexicana amastigotes similarly lacking PGs but otherwise normal in known glycoconjugates remain able to induce acute pathology. To explore this further, we tested the infectivity of a new PG-null L. major mutant, which is inactivated in the two UDP-galactose transporter genes LPG5A and LPG5B. Surprisingly this mutant did not recapitulate the phenotype of L. major lpg2 −, instead resembling the L. major lipophosphoglycan-deficient lpg1 − mutant. Metacyclic lpg5A −/lpg5B − promastigotes showed strong defects in the initial steps of macrophage infection and survival. However, after a modest delay, the lpg5A − /lpg5B − mutant induced lesion pathology in infected mice, which thereafter progressed normally. Amastigotes recovered from these lesions were fully infective in mice and in macrophages despite the continued absence of PGs. This suggests that another LPG2-dependent metabolite is responsible for the L. major amastigote virulence defect, although further studies ruled out cytoplasmic mannans. These data thus resolve the distinct phenotypes seen among lpg2 − Leishmania species by emphasizing the role of glycoconjugates other than PGs in amastigote virulence, while providing further support for the role of PGs in metacyclic promastigote virulence.
APA, Harvard, Vancouver, ISO, and other styles
33

Xu, Hong, Jun Yan, Yiming Huang, and Suzanne T. Ildstad. "The Early Rejection of Allogeneic BMC by Macrophages or NK Cells Is TRIF Signaling Dependent." Blood 120, no. 21 (November 16, 2012): 1883. http://dx.doi.org/10.1182/blood.v120.21.1883.1883.

Full text
Abstract:
Abstract Abstract 1883 The barrier for rejection of allogeneic bone marrow cells (BMC) has been attributed primarily to adaptive immunity, especially T cell immune responses. Significant progress has been made in developing immune-based nonmyeloablative conditioning strategies to achieve mixed chimerism in bone marrow transplantation (BMT) with targeting of T cells. The role of the innate immune system in BMC allorejection has not been adequately addressed. The fact that when T cells are targeted, alloengraftment requires additional conditioning from nonspecific reagents, such as irradiation and immunosuppressive drugs, suggesting the existence of another barrier. As humoral immunity is unlikely a barrier for BMC in unprimed naïve recipients, the innate immune system is most likely another barrier in BMT. The present study focused on a role for components of the innate immune response in allogeneic BMT. Using T cell-deficient (TCR-β/δ−/−) mice, we found that rejection of transplanted allogeneic BMC occurred very early, well before the time required for T cell activation and was T cell independent, suggesting an effector role for innate immune cells in BMC rejection. How the innate immune system recognizes or responds to allogeneic BMC remains unknown. Toll-like receptors (TLR) are a class of proteins that play a key role in the innate immune system. The signaling function of TLR depends on intracellular adaptors of MyD88 and/or TRIF. We have demonstrated that TRIF signaling is the innate immune signaling in BMC allorejection by showing superior engraftment in mice deficient in TRIF but not MyD88. To further determine the cell populations of innate immunity in allogeneic BMC rejection mediated through TRIF signaling, TRIF deficient (TRIFLps2/Lps2) mice were used as recipients for in vivo cytotoxicity assays after adoptive transfer of wildtype innate immune cells: macrophages or NK cells. Wildtype F4/80+ macrophages were sorted from B6 spleens and peritoneal cavities and NK1.1+ NK cells from B6 spleens. The doses of transferred NK1.1+ and F4/80+ cells were 370,000 and 140,000 per recipient, respectively. One day after transfer, 20 × 106 CFSE-labeled BALB/c target (high intensity) and internal control B6 (low intensity) BMC were injected. TRIFLps2/Lps2 mice that did not receive transferred cells and wildtype B6 mice treated with saline served as controls. As expected, donor cells were rapidly eliminated in control wildtype B6 mice and rejection was complete by day 3. The rejection of donor cells was significantly less in TRIFLps2/Lps2 mice without receiving adoptively transferred cells compared with wildtype B6 controls, from marginal significance (P = 0.04) at 3 hr to the highest significance (P = 0.0001) at day 3 after cell infusion. At day 3, the killing rates were 91.4 ± 1.4% in TRIFLps2/Lps2 mice without transferred cells and 97.6 ± 1.5% in wildtype B6 controls. The eliminating rates of donor cells were increased in TRIFLps2/Lps2 recipients that received either F4/80+ or NK1.1+ cells, and the kinetics of elimination of donor cells was shifted to resemble B6 controls with no significant difference between them at these 3 time points (P values: 0.11 to 0.87). The cytotoxicity of donor cells was significantly increased in TRIFLps2/Lps2 recipients adoptively transferred with F4/80+ or NK1.1+ cells when compared with TRIFLps2/Lps2 controls at all time points (P values: 0.038 to 0.002), except the one at 3hr when compared between TRIFLps2/Lps2 recipients received NK1.1+ cells and TRIFLps2/Lps2 controls (P = 0.058). At day 1, the killing percentages of CFSE labeled BALB/c cells were 71.0 ± 5.1%, 69.1 ± 3.9%, or 61.1 ± 5.8% in TRIFLps2/Lps2 recipients that received either F4/80+ cells, NK1.1+ cells, or none, respectively. Taken together, the restored cytotoxicity in TRIF-deficient recipients transferred with wildtype F4/80+ or NK1.1+ cells suggests that TRIF signaling is essential for macrophage- and NK cell-mediated early rejection of allogeneic BMC, and that both cell types function as non-redundant effector cells in BMC rejection. Disclosures: Ildstad: Regenerex, LLC, a biotech start-up company: Equity Ownership.
APA, Harvard, Vancouver, ISO, and other styles
34

Rajendran, Sujeevan, Jung Heo, Yong Jun Kim, Dae Heon Kim, Kisung Ko, Young Koung Lee, Seok Kwi Oh, Chul Min Kim, Jong Hyang Bae, and Soon Ju Park. "Optimization of Tomato Productivity Using Flowering Time Variants." Agronomy 11, no. 2 (February 4, 2021): 285. http://dx.doi.org/10.3390/agronomy11020285.

Full text
Abstract:
The control of flowering time is a major contributing factor to the improvement of crop yield by optimizing plant growth in a crop cycle. Genetic variants that determine flowering time can provide insights into optimizing flowering time for higher yields and other beneficial traits in tomato crops. Here, we examined a collection of flowering time variants to assess their effects on biomass and total tomato yields. Five late flowering (lf), thirteen large plant (lp), and seven floral homeotic (fh) mutants were identified as flowering time variants that could be rearranged according to leaf production in the primary shoot meristem (PSM). A flowering time continuum of mutants was translated into a positive continuum of biomass yield with more leaves, branches, and floral organs. The flowering time continuum showed an optimal curve of fruit yield, indicating a certain late flowering time as optimal for fruit yield, with the yield gradually decreasing in both directions with earlier or later flowering times. We isolated lf1, lf10, lp22, and fh13 as high-yielding genotypes with optimal flowering time, showing a new balance between the vegetative and flowering phases of tomato. Additionally, lp8, fh8, and fh15 produced extremely high biomass in leaves, axillary shoots, and floral organs due to late flowering in shoot apices with additional production of floral organs and lateral shoot. Our new late-flowering variants provide new genetic resources that can be used to optimize crop yield by fine-tuning flowering time, and future molecular studies could be conducted by revisiting our yield model.
APA, Harvard, Vancouver, ISO, and other styles
35

Grimm, Dorothee, Christian H. Eggers, Melissa J. Caimano, Kit Tilly, Philip E. Stewart, Abdallah F. Elias, Justin D. Radolf, and Patricia A. Rosa. "Experimental Assessment of the Roles of Linear Plasmids lp25 and lp28-1 of Borrelia burgdorferi throughout the Infectious Cycle." Infection and Immunity 72, no. 10 (October 2004): 5938–46. http://dx.doi.org/10.1128/iai.72.10.5938-5946.2004.

Full text
Abstract:
ABSTRACT Borrelia burgdorferi, which causes Lyme disease in humans, has an unusual genome composed of a linear chromosome and up to 21 extrachromosomal elements. Experimental data suggest that two of these elements, linear plasmids lp25 and lp28-1, play essential roles for infectivity in mice. In this study, we prove the essential natures of these two plasmids by selectively displacing lp25 or lp28-1 in an infectious wild-type clone with incompatible shuttle vectors derived from the native plasmids, rendering the respective transformants noninfectious to mice. Conversely, restoration of plasmid lp25 or lp28-1 in noninfectious clones that naturally lack the corresponding plasmid reestablished infectivity in mice. This approach establishes the ability to manipulate the plasmid content of strains by eliminating or introducing entire plasmids in B. burgdorferi and will be valuable in assessing the roles of plasmids even in unsequenced B. burgdorferi strains.
APA, Harvard, Vancouver, ISO, and other styles
36

Xu, Qilong, Sunita V. Seemanapalli, Larry Lomax, Kristy McShan, Xin Li, Erol Fikrig, and Fang Ting Liang. "Association of Linear Plasmid 28-1 with an Arthritic Phenotype of Borrelia burgdorferi." Infection and Immunity 73, no. 11 (November 2005): 7208–15. http://dx.doi.org/10.1128/iai.73.11.7208-7215.2005.

Full text
Abstract:
ABSTRACT Borrelia burgdorferi, the Lyme disease spirochete, has a genome comprised of a linear chromosome and up to 21 plasmids. Loss of plasmids is associated with decreased infectivity and pathogenicity. Sixteen transformants were generated by transforming the noninfectious clone 5A13 with the recombinant plasmid pBBE22. The transformants were classified into nine groups based on plasmid content analysis. An infectivity study revealed that all nine transformants examined, each of which represented one of the plasmid patterns, were infectious in mice with severe combined immunodeficiency (SCID) regardless of their genomic compositions. Tissue bacterial quantification revealed that the loss of plasmids significantly reduced the spirochete burden in the heart and joint tissues, not in the skin, suggesting virulence factors may be tissue specific. Four transformants containing lp28-1 induced severe arthritis in SCID mice, in contrast to the five transformants lacking lp28-1. These pathogenicity studies associated lp28-1 with an arthritic phenotype and further studies may identify factors that contribute to arthritic pathology.
APA, Harvard, Vancouver, ISO, and other styles
37

Ferreira dos Santos, Thalis, Tauá Alves Melo, Milena Evangelista Almeida, Rachel Passos Rezende, and Carla Cristina Romano. "Immunomodulatory Effects ofLactobacillus plantarumLp62 on Intestinal Epithelial and Mononuclear Cells." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/8404156.

Full text
Abstract:
Probiotic lactic acid bacteria are known for their ability to modulate the immune system. They have been shown to inhibit inflammation in experiments with animal models, cell culture, and clinical trials. The objective of this study was to elucidate the anti-inflammatory potential ofLactobacillus plantarumLp62, isolated from cocoa fermentation, in a cell culture model. Lp62 inhibited IL-8 production bySalmonellaTyphi-stimulated HT-29 cells and prevented the adhesion of pathogens to these epithelial cells. The probiotic strain was able to modulate TNF-α, IL1-β, and IL-17 secretion by J774 macrophages. J774 activation was reduced by coincubation with Lp62. PBMC culture showed significantly higher levels of CD4+CD25+T lymphocytes following treatment with Lp62. Probiotics also induced increased IL-10 secretion by mononuclear cells.L. plantarumLp62 was able to inhibit inflammatory stimulation in epithelial cells and macrophages and activated a tolerogenic profile in mononuclear cells of healthy donors. These results indicate this strain for a possible application in the treatment or prevention of inflammatory diseases.
APA, Harvard, Vancouver, ISO, and other styles
38

Sexton, Jessica A., and Joseph P. Vogel. "Regulation of Hypercompetence in Legionella pneumophila." Journal of Bacteriology 186, no. 12 (June 15, 2004): 3814–25. http://dx.doi.org/10.1128/jb.186.12.3814-3825.2004.

Full text
Abstract:
ABSTRACT Although many bacteria are known to be naturally competent for DNA uptake, this ability varies dramatically between species and even within a single species, some isolates display high levels of competence while others seem to be completely nontransformable. Surprisingly, many nontransformable bacterial strains appear to encode components necessary for DNA uptake. We believe that many such strains are actually competent but that this ability has been overlooked because standard laboratory conditions are inappropriate for competence induction. For example, most strains of the gram-negative bacterium Legionella pneumophila are not competent under normal laboratory conditions of aerobic growth at 37°C. However, it was previously reported that microaerophilic growth at 37°C allows L. pneumophila serogroup 1 strain AA100 to be naturally transformed. Here we report that another L. pneumophila serogroup 1 strain, Lp02, can also be transformed under these conditions. Moreover, Lp02 can be induced to high levels of competence by a second set of conditions, aerobic growth at 30°C. In contrast to Lp02, AA100 is only minimally transformable at 30°C, indicating that Lp02 is hypercompetent under these conditions. To identify potential causes of hypercompetence, we isolated mutants of AA100 that exhibited enhanced DNA uptake. Characterization of these mutants revealed two genes, proQ and comR, that are involved in regulating competence in L. pneumophila. This approach, involving the isolation of hypercompetent mutants, shows great promise as a method for identifying natural transformation in bacterial species previously thought to be nontransformable.
APA, Harvard, Vancouver, ISO, and other styles
39

Lin, Songbai, and C. C. Yun. "Deletion of LPA2 Attenuates Murine Colitis." Gastroenterology 140, no. 5 (May 2011): S—838. http://dx.doi.org/10.1016/s0016-5085(11)63476-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Ma, Deqin, David G. Russell, Stephen M. Beverley, and Salvatore J. Turco. "Golgi GDP-mannose Uptake RequiresLeishmania LPG2." Journal of Biological Chemistry 272, no. 6 (February 7, 1997): 3799–805. http://dx.doi.org/10.1074/jbc.272.6.3799.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

JAWORSKI, Cynthia, and Graeme WISTOW. "LP2, a differentiation-associated lipid-binding protein expressed in bovine lens." Biochemical Journal 320, no. 1 (November 15, 1996): 49–54. http://dx.doi.org/10.1042/bj3200049.

Full text
Abstract:
A 13 kDa protein from bovine lens was identified and characterized by protein microsequencing and by rapid amplification of cDNA ends (RACE) PCR. Its complete sequence shows that this protein belongs to a family of fatty acid-binding proteins (FABPs), including myelin and adipocyte P2, that are associated with cellular differentiation. The bovine lens protein, designated LP2, shows very close similarity to human epidermal FABP (eFABP) and human eFABP was detected in human lens, suggesting that the two proteins might be orthologous. Reverse transcriptase–PCR (RT–PCR) was used to compare expression patterns of LP2 with those for actin and for the differentiation markers γB-crystallin and γs-crystallin in lens. Actin was most abundant in the relatively undifferentiated epithelial cells and decreased with lens cell differentiation. In contrast γB-crystallin and γs-crystallin were detected only in fibres (nuclear and cortical respectively). LP2 transcripts were detected most abundantly in fibre cells and apparently increased with cellular differentiation. Molecular modelling confirms that the sequence of LP2 fits the tertiary template of adipocyte P2 but reveals the presence of two close pairs of cysteine residues that might be susceptible to intramolecular disulphide bond formation under appropriate oxidizing conditions. LP2 is thus another potential target for oxidative stress during cataract formation in lens.
APA, Harvard, Vancouver, ISO, and other styles
42

Eckford, Paul D. W., and Christine E. Bear. "Targeting the regulation of CFTR channels." Biochemical Journal 435, no. 2 (March 29, 2011): e1-e4. http://dx.doi.org/10.1042/bj20110461.

Full text
Abstract:
In this issue of the Biochemical Journal, Zhang et al. reveal a new strategy for modifying the regulated function of CFTR (cystic fibrosis transmembrane conductance regulator) on the apical surface of epithelial cells. Simply stated, these authors tested the idea that the cAMP-dependent channel activity of CFTR could be effectively enhanced by disruption of a protein–protein interaction which is normally inhibitory for the production of cAMP. This particular protein–protein interaction [between the PDZ motif of LPA2 (type 2 lysophosphatidic acid receptor) and the scaffold protein Nherf2 (Na+/H+ exchanger regulatory factor 2)] is localized in the CFTR interactome on the apical membrane of epithelial cells. Hence disruption of the LPA2–Nherf2 interaction should lead to a localized elevation in cAMP and, consequently, increased cAMP-dependent CFTR activity on the surface of epithelial cells. Zhang et al. confirmed these expectations for a small-molecule compound targeting the LPA2–Nherf2 interaction using relevant cultures and tissues thought to model the human respiratory epithelium. The success of this strategy depended on previous knowledge regarding the role for multiple PDZ-motif-mediated interactions in signalling (directly or indirectly) to CFTR. Given the number and diversity of such PDZ-mediated interactions, future structural and computational studies will be essential for guiding the design of specific pharmacological interventions.
APA, Harvard, Vancouver, ISO, and other styles
43

Nasrallah, Gheyath K., Elizabeth Gagnon, Dennis J. Orton, and Rafael A. Garduño. "ThehtpABoperon ofLegionella pneumophilacannot be deleted in the presence of thegroEchaperonin operon ofEscherichia coli." Canadian Journal of Microbiology 57, no. 11 (November 2011): 943–52. http://dx.doi.org/10.1139/w11-086.

Full text
Abstract:
HtpB, the chaperonin of the intracellular bacterial pathogen Legionella pneumophila , displays several virulence-related functions in vitro. To confirm HtpB’s role in vivo, host infections with an htpB deletion mutant would be required. However, we previously reported that the htpAB operon (encoding co-chaperonin and chaperonin) is essential. We attempted here to delete htpAB in a L. pneumophila strain carrying the groE operon (encoding the Escherichia coli co-chaperonin and chaperonin). The groE operon was inserted into the chromosome of L. pneumophila Lp02, and then allelic replacement of htpAB with a gentamicin resistance cassette was attempted. Although numerous potential postallelic replacement transformants showed a correct selection phenotype, we still detected htpAB by PCR and full-size HtpB by immunoblot. Southern blot and PCR analysis indicated that the gentamicin resistance cassette had apparently integrated in a duplicated htpAB region. However, we showed by Southern blot that strain Lp02, and the Lp02 derivative carrying the groE operon, have only one copy of htpAB. These results confirmed that the htpAB operon cannot be deleted, not even in the presence of the groE operon, and suggested that attempts to delete htpAB under strong phenotypic selection result in aberrant genetic recombinations that could involve duplication of the htpAB locus.
APA, Harvard, Vancouver, ISO, and other styles
44

Shih, M., H. Ma, E. Nakajima, L. L. David, M. Azuma, and T. R. Shearer. "Biochemical properties of lens-specific calpain Lp85." Experimental Eye Research 82, no. 1 (January 2006): 146–52. http://dx.doi.org/10.1016/j.exer.2005.06.011.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Lattuada, Pier Luigi. "Transpersonal Psychology as a Science." Integral Transpersonal Journal 11, no. 11 (September 2018): 26–51. http://dx.doi.org/10.32031/itibte_itj_11-lp2.

Full text
Abstract:
In this article, the author will discuss the specificities of transpersonal psychology, exploring how can offer an enormous potential to psychological science, encouraging it to widen its field of application and methods. In doing so the author will offer both some of the answers to the criticism by mainstream psychology, and those ontological and epistemological aspects on which it is based.
APA, Harvard, Vancouver, ISO, and other styles
46

Cieslik, Dietmar, and Johann Linhart. "Steiner minimal trees in Lp2." Discrete Mathematics 155, no. 1-3 (August 1996): 39–48. http://dx.doi.org/10.1016/0012-365x(94)00368-s.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

Kim, Tae-Jung, and Gi-Seong Moon. "Antimicrobial Activity of Lactobacillus plantarum LP2 against Helicobacter pylori." Journal of Food Hygiene and Safety 30, no. 4 (December 30, 2015): 372–75. http://dx.doi.org/10.13103/jfhs.2015.30.4.372.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Norris, Steven J., Jerrilyn K. Howell, Evelyn A. Odeh, Tao Lin, Lihui Gao, and Diane G. Edmondson. "High-Throughput Plasmid Content Analysis ofBorrelia burgdorferiB31 by Using Luminex Multiplex Technology." Applied and Environmental Microbiology 77, no. 4 (December 17, 2010): 1483–92. http://dx.doi.org/10.1128/aem.01877-10.

Full text
Abstract:
ABSTRACTBorrelia burgdorferi, the causative agent of Lyme disease in North America, is an invasive pathogen that causes persistent multiorgan manifestations in humans and other mammals. Genetic studies of this bacterium are complicated by the presence of multiple plasmid replicons, many of which are readily lost duringin vitroculture. The analysis ofB. burgdorferiplasmid content by plasmid-specific PCR and agarose gel electrophoresis or other existing techniques is informative, but these techniques are cumbersome and challenging to perform in a high-throughput manner. In this study, a PCR-based Luminex assay was developed for determination of the plasmid content of the strainB. burgdorferiB31. This multiplex, high-throughput method allows simultaneous detection of the plasmid contents of manyB. burgdorferistrains in a 96-well format. The procedure was used to evaluate the occurrence of plasmid loss in 44 low-passageB. burgdorferiB31 clones and in a library of over 4,000 signature-tagged mutagenesis (STM) transposon mutant clones. This analysis indicated that only 40% of the clones contained all plasmids, with (in order of decreasing frequency) lp5, lp56, lp28-1, lp25, cp9, lp28-4, lp28-2, and lp21 being the most commonly missing plasmids. These results further emphasize the need for careful plasmid analysis in Lyme diseaseBorreliastudies. Adaptations of this approach may also be useful in the evaluation of plasmid content and chromosomal gene variations in additional Lyme diseaseBorreliastrains and other organisms with variable genomes and in the correlation of these genetic differences with pathogenesis and other biological properties.
APA, Harvard, Vancouver, ISO, and other styles
49

Pallavi, Pogaku, Suresh A, Srinivas P, and Ram Reddy S. "Optimization of lipase production by Staphylococcus sp. Lp12." African Journal of Biotechnology 9, no. 6 (February 8, 2010): 882–86. http://dx.doi.org/10.5897/ajb09.1222.

Full text
APA, Harvard, Vancouver, ISO, and other styles
50

Shen, Dongya, Changhui Wang, Chuan Ma, Hakim Mellah, Xiupu Zhang, Hong Yuan, and Wenping Ren. "A novel optical waveguide LP01/LP02 mode converter." Optics Communications 418 (July 2018): 98–105. http://dx.doi.org/10.1016/j.optcom.2018.02.056.

Full text
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography