Relevant bibliographies by topics / T252A

Academic literature on the topic 'T252A'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "T252A"

1

Sono, Masanori, Roshan Perera, Shengxi Jin, Thomas M. Makris, Stephen G. Sligar, Thomas A. Bryson, and John H. Dawson. "The influence of substrate on the spectral properties of oxyferrous wild-type and T252A cytochrome P450-CAM." Archives of Biochemistry and Biophysics 436, no. 1 (April 2005): 40–49. http://dx.doi.org/10.1016/j.abb.2004.12.026.

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Wang, Binju, Chunsen Li, Kshatresh Dutta Dubey, and Sason Shaik. "Quantum Mechanical/Molecular Mechanical Calculated Reactivity Networks Reveal How Cytochrome P450cam and Its T252A Mutant Select Their Oxidation Pathways." Journal of the American Chemical Society 137, no. 23 (June 5, 2015): 7379–90. http://dx.doi.org/10.1021/jacs.5b02800.

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3

Hirao, Hajime, Devesh Kumar, and Sason Shaik. "On the identity and reactivity patterns of the “second oxidant” of the T252A mutant of cytochrome P450cam in the oxidation of 5-methylenenylcamphor." Journal of Inorganic Biochemistry 100, no. 12 (December 2006): 2054–68. http://dx.doi.org/10.1016/j.jinorgbio.2006.09.001.

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4

Kim, Sun Hee, Tran-Chin Yang, Roshan Perera, Shengxi Jin, Thomas A. Bryson, Masanori Sono, Roman Davydov, John H. Dawson, and Brian M. Hoffman. "Cryoreduction EPR and 13C, 19F ENDOR study of substrate-bound substates and solvent kinetic isotope effects in the catalytic cycle of cytochrome P450cam and its T252A mutant." Dalton Transactions, no. 21 (2005): 3464. http://dx.doi.org/10.1039/b506764m.

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5

Kim, Dong Keon, Jang-Seok Lee, Eun Young Lee, Hansol Jang, Suji Han, Hee Yeon Kim, In-Young Hwang, et al. "O-GlcNAcylation of Sox2 at threonine 258 regulates the self-renewal and early cell fate of embryonic stem cells." Experimental & Molecular Medicine 53, no. 11 (November 2021): 1759–68. http://dx.doi.org/10.1038/s12276-021-00707-7.

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AbstractSox2 is a core transcription factor in embryonic stem cells (ESCs), and O-GlcNAcylation is a type of post-translational modification of nuclear-cytoplasmic proteins. Although both factors play important roles in the maintenance and differentiation of ESCs and the serine 248 (S248) and threonine 258 (T258) residues of Sox2 are modified by O-GlcNAcylation, the function of Sox2 O-GlcNAcylation is unclear. Here, we show that O-GlcNAcylation of Sox2 at T258 regulates mouse ESC self-renewal and early cell fate. ESCs in which wild-type Sox2 was replaced with the Sox2 T258A mutant exhibited reduced self-renewal, whereas ESCs with the Sox2 S248A point mutation did not. ESCs with the Sox2 T258A mutation heterologously introduced using the CRISPR/Cas9 system, designated E14-Sox2TA/WT, also exhibited reduced self-renewal. RNA sequencing analysis under self-renewal conditions showed that upregulated expression of early differentiation genes, rather than a downregulated expression of self-renewal genes, was responsible for the reduced self-renewal of E14-Sox2TA/WT cells. There was a significant decrease in ectodermal tissue and a marked increase in cartilage tissue in E14-Sox2TA/WT-derived teratomas compared with normal E14 ESC-derived teratomas. RNA sequencing of teratomas revealed that genes related to brain development had generally downregulated expression in the E14-Sox2TA/WT-derived teratomas. Our findings using the Sox2 T258A mutant suggest that Sox2 T258 O-GlcNAc has a positive effect on ESC self-renewal and plays an important role in the proper development of ectodermal lineage cells. Overall, our study directly links O-GlcNAcylation and early cell fate decisions.
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6

Fan, Jun, Stephen J. Perry, Yinghong Gao, David A. Schwarz, and Richard A. Maki. "A Point Mutation in the Human Melanin Concentrating Hormone Receptor 1 Reveals an Important Domain for Cellular Trafficking." Molecular Endocrinology 19, no. 10 (October 1, 2005): 2579–90. http://dx.doi.org/10.1210/me.2004-0301.

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Abstract G protein-coupled receptors (GPCRs) are heptahelical integral membrane proteins that require cell surface expression to elicit their effects. The lack of appropriate expression of GPCRs may be the underlying cause of a number of inherited disorders. There is evidence that newly synthesized GPCRs must attain a specific conformation for their correct trafficking to the cell surface. In this study, we show that a single point mutation in human melanin-concentrating hormone receptor (hMCHR1) at position 255 (T255A), which is located at the junction of intracellular loop 3 and transmembrane domain 6, reduces the hMCHR1 cell surface expression level to 20% of that observed for the wild-type receptor. Most of these mutant receptors are located intracellularly, as opposed to the wild-type receptor, which is located primarily on the cell surface. Immunoprecipitation experiments show that hMCHR1-T255A has reduced glycosylation compared with the wild-type receptor and is associated with the chaperone protein, calnexin, and it colocalizes in the endoplasmic reticulum with KDEL-containing proteins. We also demonstrate that a cell-permeable small molecule antagonist of hMCHR1 can function as a pharmacological chaperone to restore cell surface expression of this and other MCHR1 mutants to wild-type levels. Once rescued, the T255A mutant couples to Gq proteins as efficiently as the wild-type receptor. These data suggest that this single mutation produces an hMCHR1 that folds incorrectly, resulting in its retention in the endoplasmic reticulum, but once rescued to the cell surface can still function normally.
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7

Akparov, Valery Kh, Vladimir I. Timofeev, Inna P. Kuranova, and Tatiana V. Rakitina. "Crystal structure of mutant carboxypeptidase T from Thermoactinomyces vulgaris with an implanted S1′ subsite from pancreatic carboxypeptidase B." Acta Crystallographica Section F Structural Biology Communications 74, no. 10 (September 19, 2018): 638–43. http://dx.doi.org/10.1107/s2053230x18011962.

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A site-directed mutagenesis method has been used to obtain the G215S/A251G/T257A/D260G/T262D mutant of carboxypeptidase T from Thermoactinomyces vulgaris (CPT), in which the amino-acid residues of the S1′ subsite are substituted by the corresponding residues from pancreatic carboxypeptidase B (CPB). It was shown that the mutant enzyme retained the broad, mainly hydrophobic selectivity of wild-type CPT. The mutant containing the implanted CPB S1′ subsite was crystallized and its three-dimensional structure was determined at 1.29 Å resolution by X-ray crystallography. A comparison of the three-dimensional structures of CPT, the G215S/A251G/T257A/D260G/T262D CPT mutant and CPB showed that the S1′ subsite of CPT has not been distorted by the mutagenesis and adequately reproduces the structure of the CPB S1′ subsite. The CPB-like mutant differs from CPB in substrate selectivity owing to differences between the two enzymes outside the S1′ subsite. Moreover, the difference in substrate specificity between the enzymes was shown to be affected by residues other than those that directly contact the substrate.
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8

Hasegawa, Takahiro, Ahmad Azlina, Purevjav Javkhlan, Chenjuan Yao, Tetsuya Akamatsu, and Kazuo Hosoi. "Novel phosphorylation of aquaporin-5 at its threonine 259 through cAMP signaling in salivary gland cells." American Journal of Physiology-Cell Physiology 301, no. 3 (September 2011): C667—C678. http://dx.doi.org/10.1152/ajpcell.00058.2011.

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Aquaporin-5 (AQP5), a water channel, plays key roles in salivary secretion. The novel phosphorylation of AQP5 was investigated by using human salivary gland (HSG) cells and mouse salivary glands. In the HSG cells stably transfected with a wild-type mouse AQP5 construct, a protein band immunoreactive with antibody against phosphorylated PKA substrate was detected in the AQP5 immunoprecipitated sample, and its intensity was enhanced by short-term treatment of the cells with 8-bromo-cAMP, forskolin, or phorbol 12-myristate 13-acetate, but not by that with A23187 calcium ionophore. Such enhancement was inhibited in the presence of H-89, a PKA inhibitor. An AQP5 mutant (AQP5-T259A) expressed by transfection of HSG cells was not recognized by anti-phosphorylated PKA substrate antibody, even when the cells were stimulated with the protein kinase activators. Immunoblotting and immunofluorescence studies using a specific antibody detecting AQP5 phosphorylated at its Thr259 demonstrated that AQP5 was rapidly and transiently phosphorylated at the apical membrane of acinar cells in the submandibular and parotid glands after administration of isoproterenol, but not pilocarpine. Furthermore, both AQP5 and AQP5-T259A were constitutively localized at the plasma membrane in HSG cells under the resting and forskolin-stimulated conditions. These results suggest that AQP5 is phosphorylated at its Thr259 by PKA through cAMP, but not Ca2+, signaling pathways, and that this phosphorylation does not contribute to AQP5 trafficking in the salivary gland cells.
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9

Pei, Yi, Hongyan Du, Juliet Singer, Courtney St. Amour, Selena Granitto, Stewart Shuman, and Robert P. Fisher. "Cyclin-Dependent Kinase 9 (Cdk9) of Fission Yeast Is Activated by the CDK-Activating Kinase Csk1, Overlaps Functionally with the TFIIH-Associated Kinase Mcs6, and Associates with the mRNA Cap Methyltransferase Pcm1 In Vivo." Molecular and Cellular Biology 26, no. 3 (February 1, 2006): 777–88. http://dx.doi.org/10.1128/mcb.26.3.777-788.2006.

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ABSTRACT Cyclin-dependent kinase 9 (Cdk9) of fission yeast is an essential ortholog of metazoan positive transcription elongation factor b (P-TEFb), which is proposed to coordinate capping and elongation of RNA polymerase II (Pol II) transcripts. Here we show that Cdk9 is activated to phosphorylate Pol II and the elongation factor Spt5 by Csk1, one of two fission yeast CDK-activating kinases (CAKs). Activation depends on Cdk9 T-loop residue Thr-212. The other CAK—Mcs6, the kinase component of transcription factor IIH (TFIIH)—cannot activate Cdk9. Consistent with the specificities of the two CAKs in vitro, the kinase activity of Cdk9 is reduced ∼10-fold by csk1 deletion, and Cdk9 complexes from csk1Δ but not csk1 + cells can be activated by Csk1 in vitro. A cdk9 T212A mutant is viable but phenocopies conditional growth defects of csk1Δ strains, indicating a role for Csk1-dependent activation of Cdk9 in vivo. A cdk9 T212A mcs6 S165A strain, in which neither Cdk9 nor Mcs6 can be activated by CAK, has a synthetic growth defect, implying functional overlap between the two CDKs, which have distinct but overlapping substrate specificities. Cdk9 forms complexes in vivo with the essential cyclin Pch1 and with Pcm1, the mRNA cap methyltransferase. The carboxyl-terminal region of Cdk9, through which it interacts with another capping enzyme, the RNA triphosphatase Pct1, is essential. Together, the data support a proposed model whereby Cdk9/Pch1—the third essential CDK-cyclin complex described in fission yeast—helps to target the capping apparatus to the transcriptional elongation complex.
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10

Rahman, N., B. M. Fullen, D. Canavan, and L. Stassen. "T252 DENTAL POST PROCEDURAL PAIN: IMPACT OF DEMOGRAPHIC FACTORS." European Journal of Pain Supplements 5, no. 1 (September 2011): 51. http://dx.doi.org/10.1016/s1754-3207(11)70170-5.

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Dissertations / Theses on the topic "T252A"

1

Chao, Rebecca. "Utilising CYP199A4 from Rhodopseudomonas palustris HaA2 for biocatalysis and mechanistic studies." Thesis, 2016. http://hdl.handle.net/2440/102745.

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The cytochrome P450 enzyme CYP199A4 from Rhodopseudomonas palustris strain HaA2 is highly specific for the regioselective oxidation of para-substituted benzoic acids. A selection of these compounds was tested with the enzyme with the aim of investigating the mechanism of different P450-catalysed reactions. These studies revealed that the binding affinity and oxidative activity of CYP199A4 is influenced by the substituent at the para-position, and that to the enzyme’s known oxidative activities (demethylation, hydroxylation, heteroatom oxidation and desaturation) can be added alkene epoxidation, alkyne oxidation and aldehyde oxidation. The active oxidants involved in these CYP199A4-catalysed oxidations were investigated using two active site mutants at the conserved acid-alcohol pair, T252A CYP199A4 [CYP199A4 subscript] and D251N CYP199A4 [CYP199A4 subscript], which should disrupt different steps of the catalytic cycle. There was a general increase in hydrogen peroxide uncoupling in the T252A CYP199A4 [CYP199A4 subscript] mutant but significant levels of product formation were observed with each substrate. The D251N mutation reduced the activity of the enzyme dramatically in all but one case, suggesting that this mutation interferes with proton delivery as expected. The elevated rate of 4-ethynylbenzoic acid oxidation by T252A CYP199A4 [CYP199A4 subscript] when compared to the wild-type enzyme suggested the involvement of Cpd 0 in alkyne oxidation, while a reduction in activity with 4-methoxybenzoic acid implicated Cpd I in demethylation. Additionally, the notable increase in product formation and coupling efficiency of D251N CYP199A4 [CYP199A4 subscript] with 4-formylbenzoic acid suggested the involvement of the peroxo-anion in aldehyde oxidation. Larger cinnamic acids and closely related substrates were also investigated with CYP199A4. The binding affinity and oxidative activity of the enzyme decreased in the order 4-methoxybenzoic acid > 4-methoxycinnamic acid > 3-(4- methoxyphenyl)propionic acid > 4-methoxyphenylacetic acid, highlighting its selectivity for a planar, benzoic acid- or cinnamic acid-like framework. The exclusive oxidation of cinnamic acids and related derivatives at the para-position further demonstrated the high regioselectivity of CYP199A4. While CYP199A4 exhibited low oxidation activity towards para-methoxy substituted benzene derivatives, considerably higher levels of activity reminiscent of the demethylation of 4-methoxybenzoic acid were observed for the Ser244 → Asp244 (S244D) mutant of CYP199A4. The exclusive demethylation of the para-methoxy substituted benzenes by S244D revealed that the regioselectivity of CYP199A4 oxidation is maintained in this mutant. The regioselectivity of the S244D mutant was further investigated using a selection of methyl- and ethyl-substituted derivatives. The methyl analogues were exclusively oxidised at the para-position to a single α-hydroxylation product. α-Hydroxylation and Cα [α subscript] -Cᵦ desaturation products were generated in the turnovers of the ethyl derivatives. The alcohol was formed with high stereoselectivity. The electronic properties of the ethyl substrates were found to influence the ratio of hydroxylation/desaturation product, with the more electron donating substrates giving rise to a greater proportion of the latter. This suggested the involvement of a cationic intermediate in CYP199A4- catalysed desaturation.
Thesis (M.Phil.) -- University of Adelaide, School of Physical Sciences, 2016.
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2

Hsu, Deng-Kai, and 許登凱. "HiDroid：Integrated Hands-on Security Labs for Android Mobile Application." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/t252ya.

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碩士
健行科技大學
資訊工程系碩士班
102
Mobile security has become increasingly important in information security since not only more and more users use smartphones as communication tools, but also hackers who see it as another way to stolen the sensitive data and gain access control. To improve the hacker defense capability of mobile network, we believe in “Learning by Doing” and think like a hacker for better security awareness as Sun Tzu’s Art of War said: 「Know the other and know yourself, fight one hundred of battles without danger」. However, hacking or pentesting in real-world is illegal and has a lot of restrictions. Visualized and Simulated hands-on-labs is a best solution for improving the capability to deal with defense strategies. In this thesis, we developed the HiDroid virtual machine. This system is a custom-made Fedora-based Linux distribution integrated with pentesting runtime environment for Android mobile app security testing to provide attackers and defenders the ability to learn, exploit, and identify design vulnerabilities and weaknesses. HiDroid comes with everything the pentester needs in order to run and test target applications – the Android emulator, Android-x86 virtual machine, AppUse ReFrameworker, development tools, SDKs, static/dynamic analysis tools, network analysis tools, intercepting proxy servers, custom-made automatic scripts, a lot of hands-on labs around the OWASP Top 10 Mobile Risks, and step-by-step practice guide.
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Books on the topic "T252A"

1

Hiemstra, David M. ITER Task T252 (1995): Gamma radiation testing of a GaAs operational amplifier for instrument applications. Mississauga, Ont: Canadian Fusion Fuels Technology Project, 1996.

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2

T282A MF Comics for Phonics Teaching Guide. Pearson Education, Limited, 2012.

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Baker, Catherine. T292A Comics for Phonics Flash Dash Blue B Set 14. Pearson Education, Limited, 2012.

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