Academic literature on the topic 'Tmp112'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Tmp112.'
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.
Journal articles on the topic "Tmp112"
1
Meija-Feldmane, Anete. "Leachates of Thermally Modified Pine (Pinus sylvestris L.) Wood." Rural Sustainability Research 34, no. 329 (December 1, 2015): 26–31. http://dx.doi.org/10.1515/plua-2015-0010.
Full textAbstract:
Abstract During the last decades, thermally modified wood has become an object of interest among the wood scientists as an environmentally friendly material, because nowadays environmental aspects of materials have become more and more significant. Leaching is one of the processes that occurs in outdoor use. The aim of this study was to evaluate concentration of potentially hazardous substances in leachates of thermally modified pine wood. Scots pine (Pinus sylvestris L.) wood was thermally modified using Wood Treatment Technology (WTT) company device at 170 °C for 1 hour (TMP170/1) and at 160 °C for 3 hours (TMP160/3) and the mass loss was calculated. Material preparation and leaching procedure was made according to standard LVS EN 84:2000. In obtained leachates, the content of sugars, acetic acid, furfural and tannic acid were determined. Results showed that the total wood mass loss was 7.1 ± 1.4% (n=20) for TMP170/1 and 4.0 ± 1.6% (n=20) for TMP160/3. The initial leaching velocity differs between both modes and is higher for TMP160/3. The velocity decreases exponentially with immersion time and reaches plateau after 7th (5 days) immersion, but leaching still continues after the 9th immersion (14 days). The main components in leachates were tannic acid and pentoses. Among all studied compounds furfural is the hardest leachable one. Thermally modified wood treated at TMP170/1 is more environmentally friendly due to less water leachable substances. It is worth looking forward by investigating volatile organic compounds emissions in the air as it also could give high impact on human health.
2
Zahin, Maryam, Shin-je Ghim, Sujita Khanal, Gregory D. Bossart, Alfred B. Jenson, and Joongho Joh. "Molecular characterization of novel mucosotropic papillomaviruses from a Florida manatee (Trichechus manatus latirostris)." Journal of General Virology 96, no. 12 (December 1, 2015): 3545–53. http://dx.doi.org/10.1099/jgv.0.000293.
Full textAbstract:
We isolated two new manatee papillomavirus (PV) types, TmPV3 and TmPV4, from a Florida manatee (Trichechus manatus latirostris). Two PV types were previously isolated from this species. TmPV1 is widely dispersed amongst manatees and a close-to-root PV; not much is known about TmPV2. The genomes of TmPV3 and TmPV4 were 7622 and 7771 bp in size, respectively. Both PVs had a genomic organization characteristic of all PVs, with one non-coding region and seven ORFs, including the E7 ORF that is absent in other cetacean PVs. Although these PVs were isolated from separate genital lesions of the same manatee, an enlarged E2/E4 ORF was found only in the TmPV4 genome. The full genome and L1 sequence similarities between TmPV3 and TmPV4 were 63.2 and 70.3 %, respectively. These genomes shared only 49.1 and 50.2 % similarity with TmPV1. The pairwise alignment of L1 nucleotide sequences indicated that the two new PVs nested in a monophyletic group of the genus Rhopapillomavirus, together with the cutaneotropic TmPV1 and TmPV2.
3
Asakura, Nobuaki, Chiharu Nakamura, and Ichiro Ohtsuka. "Homoeoallelic gene Ncc-tmp of Triticum timopheevii conferring compatibility with the cytoplasm of Aegilops squarrosa in the tetraploid wheat nuclear background." Genome 43, no. 3 (June 1, 2000): 503–11. http://dx.doi.org/10.1139/g00-009.
Full textAbstract:
A nuclear gene, Ncc-tmp1A, of Triticum timopheevii is required for the nucleus-cytoplasm (NC) compatibility in tetraploid NC hybrids with the cytoplasm of Aegilops squarrosa. A euploid NC hybrid of T. durum was previously produced by introgressing the gene from chromosome 1A of T. timopheevii. To examine the possible presence of a functional homoeoallele in the G genome of T. timopheevii, segregation of seed viability was studied as a marker phenotype in BC1s involving the two types of NC hybrids, (Ae. squarrosa) - T. timopheevii and (Ae. squarrosa) - T. turgidum. The result of these test crosses suggested that the G genome possesses a functional homoeoallele Ncc-tmp1G. Segregation of two RAPD (random amplified polymorphic DNA) markers that were closely linked to Ncc-tmp1A was further studied among the viable BC1s obtained from a test cross of (Ae. squarrosa) - T. timopheevii × T. turgidum. Some viable BC1 segregants without the markers were obtained, suggesting a limited degree of transmission of chromosome 1G carrying Ncc-tmp1G. However, a similar RAPD analysis of BC1s obtained after backcrosses of reciprocal F1s of T. timopheevii / T. turgidum with T. turgidum showed random marker segregation. Thus, it was concluded that Ncc-tmp1A is not required for compatibility with its own cytoplasm. Southern blot analysis of the euploid NC hybrid using RFLP (restriction fragment length polymorphism) markers on the homoeologous group 1 chromosomes showed that Ncc-tmp1A locates in the centromeric region.Key words: nucleus-cytoplasm (NC) compatibility, Ncc genes, Aegilops squarrosa, Triticum timopheevii, durum wheat.
4
Wu, Chung-Pu, Sabrina Lusvarghi, Jyun-Cheng Wang, Sung-Han Hsiao, Yang-Hui Huang, Tai-Ho Hung, and Suresh V. Ambudkar. "The Selective Class IIa Histone Deacetylase Inhibitor TMP195 Resensitizes ABCB1- and ABCG2-Overexpressing Multidrug-Resistant Cancer Cells to Cytotoxic Anticancer Drugs." International Journal of Molecular Sciences 21, no. 1 (December 29, 2019): 238. http://dx.doi.org/10.3390/ijms21010238.
Full textAbstract:
Multidrug resistance caused by the overexpression of the ATP-binding cassette (ABC) proteins in cancer cells remains one of the most difficult challenges faced by drug developers and clinical scientists. The emergence of multidrug-resistant cancers has driven efforts from researchers to develop innovative strategies to improve therapeutic outcomes. Based on the drug repurposing approach, we discovered an additional action of TMP195, a potent and selective inhibitor of class IIa histone deacetylase. We reveal that in vitro TMP195 treatment significantly enhances drug-induced apoptosis and sensitizes multidrug-resistant cancer cells overexpressing ABCB1 or ABCG2 to anticancer drugs. We demonstrate that TMP195 inhibits the drug transport function, but not the protein expression of ABCB1 and ABCG2. The interaction between TMP195 with these transporters was supported by the TMP195-stimulated ATPase activity of ABCB1 and ABCG2, and by in silico docking analysis of TMP195 binding to the substrate-binding pocket of these transporters. Furthermore, we did not find clear evidence of TMP195 resistance conferred by ABCB1 or ABCG2, suggesting that these transporters are unlikely to play a significant role in the development of resistance to TMP195 in cancer patients.
5
Zhang, Wei, Yinjie Guan, George Bayliss, and Shougang Zhuang. "Class IIa HDAC inhibitor TMP195 alleviates lipopolysaccharide-induced acute kidney injury." American Journal of Physiology-Renal Physiology 319, no. 6 (December 1, 2020): F1015—F1026. http://dx.doi.org/10.1152/ajprenal.00405.2020.
Full textAbstract:
Sepsis-associated acute kidney injury (SA-AKI) is associated with high mortality rates, but clinicians lack effective treatments except supportive care or renal replacement therapies. Recently, histone deacetylase (HDAC) inhibitors have been recognized as potential treatments for acute kidney injury and sepsis in animal models; however, the adverse effect generated by the use of pan inhibitors of HDACs may limit their application in people. In the present study, we explored the possible renoprotective effect of a selective class IIa HDAC inhibitor, TMP195, in a murine model of SA-AKI induced by lipopolysaccharide (LPS). Administration of TMP195 significantly reduced increased serum creatinine and blood urea nitrogen levels and renal damage induced by LPS; this was coincident with reduced expression of HDAC4, a major isoform of class IIa HDACs, and elevated histone H3 acetylation. TMP195 treatment following LPS exposure also reduced renal tubular cell apoptosis and attenuated renal expression of neutrophil gelatinase-associated lipocalin and kidney injury molecule-1, two biomarkers of tubular injury. Moreover, LPS exposure resulted in increased expression of BAX and cleaved caspase-3 and decreased expression of Bcl-2 and bone morphogenetic protein-7 in vivo and in vitro; TMP195 treatment reversed these responses. Finally, TMP195 inhibited LPS-induced upregulation of multiple proinflammatory cytokines/chemokines, including intercellular adhesion molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-α, and interleukin-1β, and accumulation of inflammatory cells in the injured kidney. Collectively, these data indicate that TMP195 has a powerful renoprotective effect in SA-AKI by mitigating renal tubular cell apoptosis and inflammation and suggest that targeting class IIa HDACs might be a novel therapeutic strategy for the treatment of SA-AKI that avoids the unintended adverse effects of a pan-HDAC inhibitor.
6
Nagesh, Narayana, Varun K. Sharma, A. Ganesh Kumar, and Edwin A. Lewis. "Effect of Ionic Strength on Porphyrin Drugs Interaction with Quadruplex DNA Formed by the Promoter Region of C-myc and Bcl2 Oncogenes." Journal of Nucleic Acids 2010 (2010): 1–9. http://dx.doi.org/10.4061/2010/146418.
Full textAbstract:
C-myc and Bcl2 are well characterized oncogenes that are capable of forming G-quadruplex structures. Promoter regions of C-myc and Bcl2 forming G-quadruplex structures are chemically synthesized and G-quadruplex structure is formed in presence of 100 mM potassium ion. Three different porphyrin drugs, namely TMPyP2, TMPyP3, and TMPyP4 are allowed to interact with quadruplex DNA complex and the site and nature of interaction are studied. Drug interactions with quadruplex DNA were carried out in different potassium ionic strengths using fluorescence spectroscopy. It is found that fluorescence hypochromicity decreases with an increase in ionic strength in the case of TMPyP4, TMPyP3, and TMPyP2. Fluorescence titration studies and Job plots indicate that four molecules of TMPyP4, two molecules of TMPyP3 and TMPyP2 are interacting with one molecule of quadruplex DNA.
7
Wang, HongBin, and Marcelo G. Kazanietz. "p23/Tmp21 Differentially Targets the Rac-GAP β2-Chimaerin and Protein Kinase C via Their C1 Domains." Molecular Biology of the Cell 21, no. 8 (April 15, 2010): 1398–408. http://dx.doi.org/10.1091/mbc.e09-08-0735.
Full textAbstract:
The C1 domains in protein kinase C (PKC) isozymes and other signaling molecules are responsible for binding the lipid second messenger diacylglycerol and phorbol esters, and for mediating translocation to membranes. Previous studies revealed that the C1 domain in α- and β-chimaerins, diacylglycerol-regulated Rac-GAPs, interacts with the endoplasmic reticulum/Golgi protein p23/Tmp21. Here, we found that p23/Tmp21 acts as a C1 domain-docking protein that mediates perinuclear translocation of β2-chimaerin. Glu227 and Leu248 in the β2-chimaerin C1 domain are crucial for binding p23/Tmp21 and perinuclear targeting. Interestingly, isolated C1 domains from individual PKC isozymes differentially interact with p23/Tmp21. For PKCε, it interacts with p23/Tmp21 specifically via its C1b domain; however, this association is lost in response to phorbol esters. These results demonstrate that p23/Tmp21 acts as an anchor that distinctively modulates compartmentalization of C1 domain-containing proteins, and it plays an essential role in β2-chimaerin relocalization. Our study also highlights the relevance of C1 domains in protein–protein interactions in addition to their well-established lipid-binding properties.
8
Asare, Yaw, Thomas A. Campbell-James, Yury Bokov, Lydia Luya Yu, Matthias Prestel, Omar El Bounkari, Stefan Roth, et al. "Histone Deacetylase 9 Activates IKK to Regulate Atherosclerotic Plaque Vulnerability." Circulation Research 127, no. 6 (August 28, 2020): 811–23. http://dx.doi.org/10.1161/circresaha.120.316743.
Full textAbstract:
Rationale: Arterial inflammation manifested as atherosclerosis is the leading cause of mortality worldwide. Genome-wide association studies have identified a prominent role of HDAC (histone deacetylase)-9 in atherosclerosis and its clinical complications including stroke and myocardial infarction. Objective: To determine the mechanisms linking HDAC9 to these vascular pathologies and explore its therapeutic potential for atheroprotection. Methods and Results: We studied the effects of Hdac9 on features of plaque vulnerability using bone marrow reconstitution experiments and pharmacological targeting with a small molecule inhibitor in hyperlipidemic mice. We further used 2-photon and intravital microscopy to study endothelial activation and leukocyte-endothelial interactions. We show that hematopoietic Hdac9 deficiency reduces lesional macrophage content while increasing fibrous cap thickness thus conferring plaque stability. We demonstrate that HDAC9 binds to IKK (inhibitory kappa B kinase)-α and β, resulting in their deacetylation and subsequent activation, which drives inflammatory responses in both macrophages and endothelial cells. Pharmacological inhibition of HDAC9 with the class IIa HDAC inhibitor TMP195 attenuates lesion formation by reducing endothelial activation and leukocyte recruitment along with limiting proinflammatory responses in macrophages. Transcriptional profiling using RNA sequencing revealed that TMP195 downregulates key inflammatory pathways consistent with inhibitory effects on IKKβ. TMP195 mitigates the progression of established lesions and inhibits the infiltration of inflammatory cells. Moreover, TMP195 diminishes features of plaque vulnerability and thereby enhances plaque stability in advanced lesions. Ex vivo treatment of monocytes from patients with established atherosclerosis reduced the production of inflammatory cytokines including IL (interleukin)-1β and IL-6. Conclusions: Our findings identify HDAC9 as a regulator of atherosclerotic plaque stability and IKK activation thus providing a mechanistic explanation for the prominence of HDAC9 as a vascular risk locus in genome-wide association studies. Its therapeutic inhibition may provide a potent lever to alleviate vascular inflammation. Graphical Abstract: A graphical abstract is available for this article.
9
Kishk, Safaa M., Rania M. Kishk, Asmaa S. A. Yassen, Mohamed S. Nafie, Nader A. Nemr, Gamal ElMasry, Salim Al-Rejaie, and Claire Simons. "Molecular Insights into Human Transmembrane Protease Serine-2 (TMPS2) Inhibitors against SARS-CoV2: Homology Modelling, Molecular Dynamics, and Docking Studies." Molecules 25, no. 21 (October 29, 2020): 5007. http://dx.doi.org/10.3390/molecules25215007.
Full textAbstract:
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), which caused novel corona virus disease-2019 (COVID-19) pandemic, necessitated a global demand for studies related to genes and enzymes of SARS-CoV2. SARS-CoV2 infection depends on the host cell Angiotensin-Converting Enzyme-2 (ACE2) and Transmembrane Serine Protease-2 (TMPRSS2), where the virus uses ACE2 for entry and TMPRSS2 for S protein priming. The TMPRSS2 gene encodes a Transmembrane Protease Serine-2 protein (TMPS2) that belongs to the serine protease family. There is no crystal structure available for TMPS2, therefore, a homology model was required to establish a putative 3D structure for the enzyme. A homology model was constructed using SWISS-MODEL and evaluations were performed through Ramachandran plots, Verify 3D and Protein Statistical Analysis (ProSA). Molecular dynamics simulations were employed to investigate the stability of the constructed model. Docking of TMPS2 inhibitors, camostat, nafamostat, gabexate, and sivelestat, using Molecular Operating Environment (MOE) software, into the constructed model was performed and the protein-ligand complexes were subjected to MD simulations and computational binding affinity calculations. These in silico studies determined the tertiary structure of TMPS2 amino acid sequence and predicted how ligands bind to the model, which is important for drug development for the prevention and treatment of COVID-19.
10
Liu, Shengchun, Si Zhang, Kelley Bromley-Brits, Fang Cai, Weihui Zhou, Kun Xia, Jill Mittelholtz, and Weihong Song. "Transcriptional Regulation of TMP21 by NFAT." Molecular Neurodegeneration 6, no. 1 (2011): 21. http://dx.doi.org/10.1186/1750-1326-6-21.
Full textDissertations / Theses on the topic "Tmp112"
1
Novák, Jan. "Centrála pro dálkové měření teploty." Master's thesis, Vysoké učení technické v Brně. Fakulta informačních technologií, 2012. http://www.nusl.cz/ntk/nusl-236593.
Full textAbstract:
This master's thesis deals with wireless sensor network and temperature sensors with aim to design and implement remote temperature sensing central based on mesh topology. This paper discuss components of board modules, their function, and principles of RF PCB design. It describes the development tools and application displaying measured values.
2
Fazi, Davide. "Progetto di un nodo sensore a nanocorrenti basato su microcontrollore." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2017. http://amslaurea.unibo.it/13141/.
Full textAbstract:
Le prestazioni e la densità di integrazione dei circuiti integrati hanno avuto una incredibile crescita negli ultimi decenni.
Questo incredibile sviluppo ha portato ad una enorme crescita delle applicazioni dei circuiti elettronici, fino ad arrivare a pensare di poter rendere “smart” e connesso ad Internet ogni oggetto di uso comune, grazie alla cosiddetta “Internet of Things”.
In questo panorama trovano dunque sempre maggior spazio i sensori, indispensabili al fine di monitorare i parametri d’interesse negli oggetti da controllare.
Un altro aspetto molto importante è quello di ridurre il consumo dei dispositivi. Gli oggetti da connettere ad internet nella maggior parte dei casi saranno infatti da alimentare a batteria.
Lo scopo di questo elaborato è quello di sviluppare un nodo sensore con annesso un datalogger mediante l’utilizzo di un microcontrollore. L’obiettivo principale è di ridurne il consumo al minimo, con correnti di standby dell’ordine delle decine di nA, così da poter alimentare tale circuito per un periodo di diversi anni con la batteria più piccola possibile.
Il circuito sarà non solo progettato ma anche realizzato su PCB, al fine di poterne collaudare il funzionamento reale e di poterlo confrontare con quello previsto.
Un dispositivo di questo tipo, oltre ad essere un utile caso di studio per mostrare i valori minimi di consumo verso i quali sia possibile spingersi, potrebbe trovare applicazione in situazioni in cui si renda necessario monitorare determinati parametri in condizioni tali da rendere difficoltosa la sostituzione della batteria e quindi anche il monitoraggio real-time che richiederebbe necessariamente un maggior consumo.
Il progetto si compone di un microcontrollore che, oltre a gestire la lettura di un sensore, si occupa di implementare la funzione di datalogger. Un altro componente fondamentale è un timer, avente lo scopo di gestire il periodo di attività del µC.
3
Bromley-Brits, Kelley. "TMP21 in Alzheimer's disease : biochemical and behavioural characterization of TMP21." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34670.
Full textAbstract:
Alzheimer's disease (AD) is the most common neurodegenerative disorder leading to dementia. The two major neuropathological hallmarks of AD are the deposition
of amyloid-b (Ab) protein in neuritic plaques and the formation of neuro brillary tangles. Ab is generated from a larger Ab recursor protein (APP) following sequential cleavage by b- and g-secretase. APP can also be cleaved in a non-amyloidogenic
pathway following sequential cleavage by a- and g-secretase. In addition to the pathogenic processing of APP, the g-secretase complex also cleaves a protein called Notch, which is essential for embryonic development and may be involved in learning
and memory. Transmembrane emp24-like trafficking protein 10 (TMP21) is a 21 kDa transmembrane
protein involved in vesicular trafficking. Ubiquitously expressed, particularly in the plasma membrane, endoplasmic reticulum, and Golgi, TMP is vital to development, and homozygous knockout mice are embryonic lethal. Recently, TMP21 was found to play a second, pivotal role as a regulatory member of the
g-secretase complex involved in AD pathogenesis. Knockdown of TMP21 increased Ab production without affecting Notch cleavage, making it a seductive target for
AD research (Chen et al., 2006).
This thesis shows that, similar to other members of the g-secretase complex, TMP21 is also degraded by the ubiquitin-proteasome pathway, as treatment with proteasomal inhibitors increased TMP21 protein levels in both a time- and dose-dependent manner. Furthermore, overexpression of TMP21 shifted APP processing
from the a-secretase to b-secretase pathway in cell culture, and b-secretase and
TMP21 could coimmunoprecipitate. This suggests that TMP21 may not only a ffect AD pathogenesis through its modulatory role on g-secretase or its trafficking of
APP (Vetrivel et al., 2007), but also through its influence on b-secretase, providing a novel enzymatic target for future study.
Finally, this work presents the only in vivo study of the behavioural consequences
of TMP21 suppression. Motor function, anxiety, and learning and memory were examined using a comprehensive test battery. Mice heterozygous for TMP21 were
found to have slightly enhanced physical abilities, increased anxiety, and potential anxiety-augmented de ficits in hippocampal learning and memory. This data will
prove vital when examining future work regarding TMP21 suppression in a mouse model of AD.
4
Zhang, Xiaojie. "Roles of TMP21 in Alzheimer's disease." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50490.
Full textAbstract:
Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the unique pathological feature of Alzheimer’s disease (AD). Aβ is derived from the cleavages of amyloid β precursor protein (APP) by β-secretase at Asp-1 site and by γ-secretase. Beta-site APP cleaving enzyme 1 (BACE1) is the β-secretase. It mainly cleaves APP within the Aβ region at the Glu-11 site to generate truncated Aβ species. Twenty-one kilodalton transmembrane trafficking protein, TMP21 (also named TMED10, p23) is a vesicular trafficking protein and a member of p24 family proteins. TMP21 mediates protein endoplasmic reticulum (ER)/Golgi transport and selectively guides the glycosylphosphatidylinositol-anchored proteins into lipid rafts. It is also essential for forming Golgi structural organization. Recent studies show that the downregulation of TMP21 increases Aβ generation by affecting APP trafficking and selectively modulating γ-cleavage on APP. However, the precise roles of TMP21 in AD pathogenesis remain unknown.
In this thesis, we reported the discovery of a novel AD-associated single nucleotide polymorphism (SNP) in the intron 4 of Tmp21. This SNP significantly increases TMP21 transcript splicing efficiency in vitro, resulting in upregulation of TMP21 gene expression. Furthermore, we found that overexpression of TMP21 shifts APP processing from the non-amyloidogenic to the amyloidogenic pathway by specifically increasing the BACE1 activity at Asp-1 site. Downregulation of TMP21 also facilitates amyloidogenic cleavage. The interaction between TMP21 and BACE1 is essential for BACE1’s ER export, and TMP21 enhances APP/BACE1 co-residency and might guide both APP and immature BACE1 in lipid rafts-like structures.
In summary, this study defined the roles of TMP21 in AD pathogenesis. It demonstrated for the first time the genetic association between TMP21 and AD. The study also found that TMP21 facilitates APP amyloidogenic processing by modulating BACE1 maturation and trafficking, leading to increased BACE1 cleavage at Asp-1 site to generate Aβ. Therefore, interrupting the interaction between TMP21 and BACE1 to reduce Aβ production could be potential strategy to develop drugs for treating AD.Medicine, Faculty of
Graduate
5
Kutanovas, Simonas. "Tetrametilpirazino skaidymo Rhodococcus sp. TMP1 bakterijose tyrimas." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2013. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2013~D_20130701_092234-05318.
Full textAbstract:
Alkilpirazinų katabolizmas bakterijose yra prastai ištirtas. Nors yra žinomi tarpiniai metabolitai susidarantys skaidant di- ir tri- pakeistus alkilpirazinus, tačiau šių junginių skaidymas prasideda hidroksilinimo reakcija, kuri negalima tetrametilpirazino atveju. Šiame darbe pirmą kartą nustatytas tetrametilpirazino katabolizmo kelias šį junginį skaidančiose Rhodococcus jostii TMP1 bakterijose. MS/MS de novo sekoskaitos būdu identifikavus tetrametilpirazinu indukuojamą baltymą, buvo nustatyta genų sankaupa, koduojanti pradines tetrametilpirazino katabolizmo reakcijas katalizuojančius fermentus ir transkripcijos reguliatorių, dalyvaujantį šių genų aktyvavime. Pradiniame tetrametilpirazino skaidymo etape monooksigenazė TpdAB katalizuoja oksidacinį žiedo atidarymą, susidarant (Z)-N,N'-(but-2-ene-2,3-diil)diacetamidui. Tolesnę skaidymo reakciją katalizuoja amidazė TpdC, kurios produktą N-(3-oksobutan-2-il)acetamidą aminoalkoholių dehidrogenazė TpdE redukuoja iki N-(3-hidroksibutan-2-il)acetamido. Nustačius tarpinius tetrametilpirazino skaidymo metabolitus, reakcijas katalizuojančius fermentus ir juos koduojančius genus buvo rekonstruotas pirmasis alkilpirazinų katabolizmo kelias bakterijose. Darbo metu taip pat parodyta, kad Rhodococcus jostii TMP1 bakterijos modifikuoja daugelį alkilpirazino ir alkilpiridino junginių ir gali būti panaudotos 2,4,6-trimetilpiridin-3-olio biosintezei iš 2,4,6-trimetilpiridino.The catabolism of alkylpyrazines is poorly described. The pathways for the degradation of di- and tri-substituted pyrazines have been proposed, but these related routes consistently include a hydroxylation step that cannot be performed on tetramethylpyrazine. Here we describe for the first time the catabolic pathway of tetramethylpyrazine in tetramethylpyrazine-degrading Rhodococcus jostii TMP1 strain. MS/MS analysis of the protein primarily upregulated by tetramethylpyrazine led to the identification of the gene locus encoding proteins required for the initial steps of tetrametylpyrazine degradation and for the regulation of this locus. Tetramethylpyrazine degradation starts with oxidative ring cleavage catalysed by monooxygenase TpdAB, which produces (Z)-N,N'-(but-2-ene-2,3-diyl)diacetamide. This compound is further hydrolysed by amidase TpdC to N-(3-oxobutan-2-yl)acetamide. TpdE was confirmed to be an aminoalcohol dehydrogenase yielding N-(3-hydroxybutan-2-yl)acetamide. By determining intermediates, enzymes involved and genes responsible for tetramethylpyrazine degradation we provide the first validated pathway for pyrazine degradation. We also report that Rhodococcus jostii TMP1 is capable of modifying various alkylpyrazines and alkylpyridines and can be employed for the bioconversion of 2,4,6-trimethylpyridine and 2,4,6-trimethylpyridin-3-ol biosynthesis.
6
Kutanovas, Simonas. "Investigation of tetramethylpyrazine degradation in Rhodococcus sp. TMP1 bacteria." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2013. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2013~D_20130701_092345-19015.
Full textAbstract:
The catabolism of alkylpyrazines is poorly described. The pathways for the degradation of di- and tri-substituted pyrazines have been proposed, but these related routes consistently include a hydroxylation step that cannot be performed on tetramethylpyrazine. Here we describe for the first time the catabolic pathway of tetramethylpyrazine in tetramethylpyrazine-degrading Rhodococcus jostii TMP1 strain. MS/MS analysis of the protein primarily upregulated by tetramethylpyrazine led to the identification of the gene locus encoding proteins required for the initial steps of tetrametylpyrazine degradation and for the regulation of this locus. Tetramethylpyrazine degradation starts with oxidative ring cleavage catalysed by monooxygenase TpdAB, which produces (Z)-N,N'-(but-2-ene-2,3-diyl)diacetamide. This compound is further hydrolysed by amidase TpdC to N-(3-oxobutan-2-yl)acetamide. TpdE was confirmed to be an aminoalcohol dehydrogenase yielding N-(3-hydroxybutan-2-yl)acetamide. By determining intermediates, enzymes involved and genes responsible for tetramethylpyrazine degradation we provide the first validated pathway for pyrazine degradation. We also report that Rhodococcus jostii TMP1 is capable of modifying various alkylpyrazines and alkylpyridines and can be employed for the bioconversion of 2,4,6-trimethylpyridine and 2,4,6-trimethylpyridin-3-ol biosynthesis.Alkilpirazinų katabolizmas bakterijose yra prastai ištirtas. Nors yra žinomi tarpiniai metabolitai susidarantys skaidant di- ir tri- pakeistus alkilpirazinus, tačiau šių junginių skaidymas prasideda hidroksilinimo reakcija, kuri negalima tetrametilpirazino atveju. Šiame darbe pirmą kartą nustatytas tetrametilpirazino katabolizmo kelias šį junginį skaidančiose Rhodococcus jostii TMP1 bakterijose. MS/MS de novo sekoskaitos būdu identifikavus tetrametilpirazinu indukuojamą baltymą, buvo nustatyta genų sankaupa, koduojanti pradines tetrametilpirazino katabolizmo reakcijas katalizuojančius fermentus ir transkripcijos reguliatorių, dalyvaujantį šių genų aktyvavime. Pradiniame tetrametilpirazino skaidymo etape monooksigenazė TpdAB katalizuoja oksidacinį žiedo atidarymą, susidarant (Z)-N,N'-(but-2-ene-2,3-diil)diacetamidui. Tolesnę skaidymo reakciją katalizuoja amidazė TpdC, kurios produktą N-(3-oksobutan-2-il)acetamidą aminoalkoholių dehidrogenazė TpdE redukuoja iki N-(3-hidroksibutan-2-il)acetamido. Nustačius tarpinius tetrametilpirazino skaidymo metabolitus, reakcijas katalizuojančius fermentus ir juos koduojančius genus buvo rekonstruotas pirmasis alkilpirazinų katabolizmo kelias bakterijose. Darbo metu taip pat parodyta, kad Rhodococcus jostii TMP1 bakterijos modifikuoja daugelį alkilpirazino ir alkilpiridino junginių ir gali būti panaudotos 2,4,6-trimetilpiridin-3-olio biosintezei iš 2,4,6-trimetilpiridino.
7
Lee, Lydia. "Localization and characterization of the regulatory regions involved in TMP1 expression." Thesis, 1988. http://spectrum.library.concordia.ca/3614/1/ML44832.pdf.
Full text
8
Jackson, Carlo Stephan. "Significance of photosynthesis and the photosynthesis related genes TMP14, FBPase and P700 in Russian wheat aphid resistant wheat." Diss., 2010. http://hdl.handle.net/2263/29033.
Full text
9
Ord, Robin. "Periodic expression of the TMP1 gene of Saccharomyces cerevisiae which encodes thymidylate synthase." Thesis, 1987. http://spectrum.library.concordia.ca/3909/1/NL37091.pdf.
Full text
10
Wang, Jyun Cheng, and 王俊程. "Investigating the chemosensitizing effect of TMP195, a HDAC class IIa inhibitor and avapritinib, a dual inhibitor of PDGFRα and KIT, in human multidrug resistant cancer cells overexpressing ABCB1 or ABCG2." Thesis, 2019. http://ndltd.ncl.edu.tw/cgi-bin/gs32/gsweb.cgi/login?o=dnclcdr&s=id=%22107CGU05114080%22.&searchmode=basic.
Full textConference papers on the topic "Tmp112"
1
Vanderwall, E. R., K. A. Barrow, L. M. Rich, S. R. Reeves, M. P. White, N. D. Sather, W. E. Harrington, and J. S. Debley. "Relationship Between Ace2 and Tmprr2 Expression by Differentiated Primary Bronchial Airway Epithelial Cells and SarsCoV2 Replication." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1281.
Full text
2
Wang, Hongbin, Liqing Xiao, and Marcelo G. Kazanietz. "Abstract 194: The Golgi/ER protein p23/Tmp21 regulates PKCΔ-mediated apoptosis in prostate cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-194.
Full text