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Journal articles on the topic 'Α-TTP'

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Published: 3 June 2025

Last updated: 31 July 2025

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1

Yoshitomo, Taguchi, Komatsu-Tanaka Mari, Hirose Norie, Kaji Yurie та Saeki Kazuhiro. "Molecular Cloning and Expression Analysis of Bovine Alpha-tocopherol Transfer Protein (α-TTP)". Annual Research & Review in Biology 12, № 5 (2017): 1–7. https://doi.org/10.9734/ARRB/2017/33400.

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<strong>Aims:</strong> To understand the mechanisms by which cattle circulate and accumulate vitamin E, we cloned the cDNA for bovine α-tocopherol transfer protein (α-TTP) and examined its expression in different tissues. <strong>Methodology:</strong> A full length α-TTP cDNA was amplified from bovine liver by RT-PCR. Poly (A)<sup>+</sup> RNA obtained from bovine tissues was subjected to RT-PCR analysis to examine α-TTP mRNA expression. Western blot analysis was performed using polyclonal antibody raised against an oligopeptide derived from bovine α-TTP to examine α-TTP protein expression in v

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2

Chung, Stacey, Mikel Ghelfi, Jeffrey Atkinson та ін. "Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein". Journal of Biological Chemistry 291, № 33 (2016): 17028–39. http://dx.doi.org/10.1074/jbc.m116.734210.

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α-Tocopherol (vitamin E) is an essential nutrient for all vertebrates. From the eight naturally occurring members of the vitamin E family, α-tocopherol is the most biologically active species and is selectively retained in tissues. The hepatic α-tocopherol transfer protein (TTP) preferentially selects dietary α-tocopherol and facilitates its transport through the hepatocyte and its secretion to the circulation. In doing so, TTP regulates body-wide levels of α-tocopherol. The mechanisms by which TTP facilitates α-tocopherol trafficking in hepatocytes are poorly understood. We found that the int

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3

FECHNER, Henry, Michael SCHLAME, Florian GUTHMANN, Paul A. STEVENS та Bernd RÜSTOW. "α- and δ-tocopherol induce expression of hepatic α-tocopherol-transfer-protein mRNA". Biochemical Journal 331, № 2 (1998): 577–81. http://dx.doi.org/10.1042/bj3310577.

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α-Tocopherol transfer protein (α-TTP) supplements nascent very-low-density lipoprotein (VLDL) preferentially with α-tocopherol by selecting the α-isomers against other stereoisomers of tocopherol. It is exclusively expressed in liver. We investigated whether the expression of the hepatic α-TTP can be induced by dietary tocopherols. Vitamin E-depleted rats were fed with a diet containing α- and δ-tocopherol (ratio 1:3). The expression of α-TTP mRNA was measured in liver tissue. The ratio of tocopherol stereoisomers was determined in plasma, plasma lipoproteins and tissues to measure the metabol

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4

Carballo, Ester, та Perry J. Blackshear. "Roles of tumor necrosis factor-α receptor subtypes in the pathogenesis of the tristetraprolin-deficiency syndrome". Blood 98, № 8 (2001): 2389–95. http://dx.doi.org/10.1182/blood.v98.8.2389.

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Abstract Tristetraprolin (TTP) is a member of the CCCH tandem zinc-finger class of proteins. It can bind to and destabilize mRNAs encoding tumor necrosis factor-α (TNF-α) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Conversely, mice deficient in TTP develop a complex syndrome characterized by cachexia, myeloid hyperplasia, and joint and skin inflammation. Studies using anti–TNF-α neutralizing antibodies demonstrated that this syndrome, at least in part, is a consequence of the excess production of TNF-α in the absence of TTP. To evaluate the role played by each TNF-α receptor

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5

Lai, Wi S., Ester Carballo, Julie R. Strum, Elizabeth A. Kennington, Ruth S. Phillips, and Perry J. Blackshear. "Evidence that Tristetraprolin Binds to AU-Rich Elements and Promotes the Deadenylation and Destabilization of Tumor Necrosis Factor Alpha mRNA." Molecular and Cellular Biology 19, no. 6 (1999): 4311–23. http://dx.doi.org/10.1128/mcb.19.6.4311.

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ABSTRACT Mice deficient in tristetraprolin (TTP), the prototype of a family of CCCH zinc finger proteins, develop an inflammatory syndrome mediated by excess tumor necrosis factor alpha (TNF-α). Macrophages derived from these mice oversecrete TNF-α, by a mechanism that involves stabilization of TNF-α mRNA, and TTP can bind directly to the AU-rich element (ARE) in TNF-α mRNA (E. Carballo, W. S. Lai, and P. J. Blackshear, Science 281:1001–1005, 1998). We show here that TTP binding to the TNF-α ARE is dependent upon the integrity of both zinc fingers, since mutation of a single cysteine residue i

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6

Irías-Mata, Andrea, Nadine Sus, Maria-Lena Hug, Marco Müller, Walter Vetter та Jan Frank. "α-Tocomonoenol Is Bioavailable in Mice and May Partly Be Regulated by the Function of the Hepatic α-Tocopherol Transfer Protein". Molecules 25, № 20 (2020): 4803. http://dx.doi.org/10.3390/molecules25204803.

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Tocomonoenols are vitamin E derivatives present in foods with a single double bond at carbon 11’ in the sidechain. The α-tocopherol transfer protein (TTP) is required for the maintenance of normal α-tocopherol (αT) concentrations. Its role in the tissue distribution of α-11′-tocomonoenol (αT1) is unknown. We investigated the tissue distribution of αT1 and αT in wild-type (TTP+/+) and TTP knockout (TTP−/−) mice fed diets with either αT or αT1 for two weeks. αT1 was only found in blood, not tissues. αT concentrations in TTP+/+ mice were in the order of adipose tissue > brain > heart > s

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7

Du, Guodong, and L. Keith Woo. "Alcohol oxidation with dioxygen mediated by oxotitanium porphyrin and related transition metal complexes." Journal of Porphyrins and Phthalocyanines 09, no. 03 (2005): 206–13. http://dx.doi.org/10.1142/s1088424605000277.

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Oxotitanium porphyrin ( TTP ) Ti = O and related transition metal complexes were shown to catalyze the oxidation of alcohols using dioxygen as the oxidant. Vicinal diols were cleaved to carbonyl compounds in the presence of catalytic amounts of ( TTP ) Ti = O , ( TTP ) V = O or ( Saldach ) V = O . α-Hydroxy ketones were oxidized to α-diketones with ( TTP ) Ti = O . Benzyl alcohol was converted to benzaldehyde in modest to high yields by a number of high valent transition metal complexes. Reaction pathways for the transformations mediated by ( TTP ) Ti = O are discussed. Formation of diolato an

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8

Smoak, Kathleen, and John A. Cidlowski. "Glucocorticoids Regulate Tristetraprolin Synthesis and Posttranscriptionally Regulate Tumor Necrosis Factor Alpha Inflammatory Signaling." Molecular and Cellular Biology 26, no. 23 (2006): 9126–35. http://dx.doi.org/10.1128/mcb.00679-06.

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ABSTRACT Glucocorticoids are used to treat various inflammatory disorders, but the mechanisms underlying these actions are incompletely understood. The zinc finger protein tristetraprolin (TTP) destabilizes several proinflammatory cytokine mRNAs by binding to AU-rich elements within their 3′ untranslated regions, targeting them for degradation. Here we report that glucocorticoids induce the synthesis of TTP mRNA and protein in A549 lung epithelial cells and in rat tissues. Dexamethasone treatment leads to a sustained induction of TTP mRNA expression that is abrogated by RU486. Glucocorticoid i

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9

Sun, Lei, Georg Stoecklin, Susan Van Way, et al. "Protein Phosphatase 2A destabilizes TNF alpha mRNA by dephosphorylating Tristetraprolin (94.8)." Journal of Immunology 178, no. 1_Supplement (2007): S172. http://dx.doi.org/10.4049/jimmunol.178.supp.94.8.

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Abstract Tumor necrosis factor (TNF)-α is a major cytokine produced by alveolar macrophages in response to pathogen associated molecular patterns such as LPS. TNF-α secretion is regulated at both transcriptional and post-transcriptional levels. Post-transcriptional regulation occurs by modulation of TNF-α mRNA stability via the binding of tristetraprolin (TTP) to the AU (adenosine/uridine)-rich elements (AREs) found in the 3’-untranslated region (3’-UTR) of TNF-α transcript. Phosphorylation plays important roles in modulating mRNA stability. Our results show that inhibition of PP2A by okadaic

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10

Chiroma, Aishatu Ali, Huzwah Khaza’ai, Roslida Abd. Hamid, Sui Kiat Chang, Zainul Amiruddin Zakaria та Zaida Zainal. "Analysis of expression of vitamin E-binding proteins in H2O2 induced SK-N-SH neuronal cells supplemented with α-tocopherol and tocotrienol-rich fraction". PLOS ONE 15, № 11 (2020): e0241112. http://dx.doi.org/10.1371/journal.pone.0241112.

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Natural α-tocopherol (α-TCP), but not tocotrienol, is preferentially retained in the human body. α-Tocopherol transfer protein (α-TTP) is responsible for binding α-TCP for cellular uptake and has high affinity and specificity for α-TCP but not α-tocotrienol. The purpose of this study was to examine the modification of α-TTP together with other related vitamin E-binding genes (i.e., TTPA, SEC14L2, and PI-TPNA) in regulating vitamin E uptake in neuronal cells at rest and under oxidative stress. Oxidative stress was induced with H2O2 for an hour which was followed by supplementation with differen

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11

Mahtani, Kamal R., Matthew Brook, Jonathan L. E. Dean, Gareth Sully, Jeremy Saklatvala, and Andrew R. Clark. "Mitogen-Activated Protein Kinase p38 Controls the Expression and Posttranslational Modification of Tristetraprolin, a Regulator of Tumor Necrosis Factor Alpha mRNA Stability." Molecular and Cellular Biology 21, no. 19 (2001): 6461–69. http://dx.doi.org/10.1128/mcb.21.9.6461-6469.2001.

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ABSTRACT Signal transduction pathways regulate gene expression in part by modulating the stability of specific mRNAs. For example, the mitogen-activated protein kinase (MAPK) p38 pathway mediates stabilization of tumor necrosis factor alpha (TNF-α) mRNA in myeloid cells stimulated with bacterial lipopolysaccharide (LPS). The zinc finger protein tristetraprolin (TTP) is expressed in response to LPS and regulates the stability of TNF-α mRNA. We show that stimulation of RAW264.7 mouse macrophages with LPS induces the binding of TTP to the TNF-α 3′ untranslated region. The p38 pathway is required

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12

Zhang, T., V. Kruys, G. Huez, and C. Gueydan. "AU-rich element-mediated translational control: complexity and multiple activities of trans-activating factors." Biochemical Society Transactions 30, no. 6 (2002): 952–58. http://dx.doi.org/10.1042/bst0300952.

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Tumour necrosis factor (TNF)-α mRNA contains an AU-rich element (ARE) in its 3′ untranslated region (3′UTR), which determines its half-life and translational efficiency. In unstimulated macrophages, TNF-α mRNA is repressed translationally, and becomes efficiently translated upon cell activation. Gel retardation experiments and screening of a macrophage cDNA expression library with the TNF-α ARE allowed the identification of TIA-1-related protein (TIAR), T-cell intracellular antigen-1 (TIA-1) and tristetraprolin (TTP) as TNF-α ARE-binding proteins. Whereas TIAR and TIA-1 bind the TNF-α ARE inde

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13

Suzuki, Hiroshi, Aiko Kume та Maria Herbas. "Potential of Vitamin E Deficiency, Induced by Inhibition of α-Tocopherol Efflux, in Murine Malaria Infection". International Journal of Molecular Sciences 20, № 1 (2018): 64. http://dx.doi.org/10.3390/ijms20010064.

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Although epidemiological and experimental studies have suggested beneficial effects of vitamin E deficiency on malaria infection, it has not been clinically applicable for the treatment of malaria owing to the significant content of vitamin E in our daily food. However, since α-tocopherol transfer protein (α-TTP) has been shown to be a determinant of vitamin E level in circulation, manipulation of α-tocopherol levels by α-TTP inhibition was considered as a potential therapeutic strategy for malaria. Knockout studies in mice indicated that inhibition of α-TTP confers resistance against malaria

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14

Shi, Jia-Xin, Xin Su, Jin Xu, Wei-Yun Zhang та Yi Shi. "MK2 posttranscriptionally regulates TNF-α-induced expression of ICAM-1 and IL-8 via tristetraprolin in human pulmonary microvascular endothelial cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 302, № 8 (2012): L793—L799. http://dx.doi.org/10.1152/ajplung.00339.2011.

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Tristetraprolin (TTP), a substrate of p38 mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MK2), is an RNA-binding protein that binds to AU-rich elements (AREs) in the 3′-untranslated region (3′-UTR) of its target mRNAs and accelerates mRNA degradation. A previous study by our group showed that MK2 regulates tumor necrosis factor-α (TNF-α)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) in human lung microvascular endothelial cells; however, the downstream protein of MK2 remains unknown. Interestingly, both ICAM-1 and IL-8 have AREs

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15

Mattijssen, Sandy, and Richard J. Maraia. "LARP4 Is Regulated by Tumor Necrosis Factor Alpha in a Tristetraprolin-Dependent Manner." Molecular and Cellular Biology 36, no. 4 (2015): 574–84. http://dx.doi.org/10.1128/mcb.00804-15.

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LARP4 is a protein with unknown function that independently binds to poly(A) RNA, RACK1, and the poly(A)-binding protein (PABPC1). Here, we report on its regulation. We found a conserved AU-rich element (ARE) in the human LARP4 mRNA 3′ untranslated region (UTR). This ARE, but not its antisense version or a point-mutated version, significantly decreased the stability of β-globin reporter mRNA. We found that overexpression of tristetraprolin (TTP), but not its RNA binding mutant or the other ARE-binding proteins tested, decreased cellular LARP4 levels. RNA coimmunoprecipitation showed that TTP s

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16

Frenzel, Laurent, Noha Semaan, Ghada Alsaleh, Dominique Wachsmann, Jacques-Eric Gottenberg, and Jean Sibilia. "A new mode of TNF-[alpha] inhibition by microRNA (99.26)." Journal of Immunology 182, no. 1_Supplement (2009): 99.26. http://dx.doi.org/10.4049/jimmunol.182.supp.99.26.

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Abstract TNF-α, is a major cytokine implicated in rheumatoid arthritis (RA). TNF-α expression is regulated both at the transcriptional and the postranscriptional levels and recent data demonstrated that miRNAs are implicated in TNF-α response in macrophages. LPS-activated synoviocytes fibroblast-like (FLS) isolated from RA patients express TNF-α mRNA but they do not release TNF-α. This inhibition is due to a rapid degradation of TNF-α mRNA. We demonstrated previously that miR-346, which is overexpressed in LPS-activated FLS inhibits Bruton's tyrosine kinase (Btk) expression, which controls TNF

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17

Chao, Pei-Min, Wan-Hsuan Chen, Chun-Huei Liao та Huey-Mei Shaw. "Conjugated Linoleic Acid Causes a Marked Increase in Liver α-Tocopherol and Liver α-Tocopherol Transfer Protein in C57BL/6 J Mice". International Journal for Vitamin and Nutrition Research 80, № 1 (2010): 65–73. http://dx.doi.org/10.1024/0300-9831/a000007.

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Conjugated linoleic acid (CLA) is a collective term for the positional and geometric isomers of a conjugated diene of linoleic acid (C18:2, n-6). The aims of the present study were to evaluate whether levels of hepatic α-tocopherol, α-tocopherol transfer protein (α-TTP), and antioxidant enzymes in mice were affected by a CLA-supplemented diet. C57BL/6 J mice were divided into the CLA and control groups, which were fed, respectively, a 5 % fat diet with or without 1 g/100 g of CLA (1:1 mixture of cis-9, trans-11 and trans-10, cis-12) for four weeks. α-Tocopherol levels in plasma and liver were

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18

Suzuki, Kotaro, Hiroshi Nakajima, Kei Ikeda та ін. "IL-4–Stat6 Signaling Induces Tristetraprolin Expression and Inhibits TNF-α Production in Mast Cells". Journal of Experimental Medicine 198, № 11 (2003): 1717–27. http://dx.doi.org/10.1084/jem.20031701.

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Increasing evidence has revealed that mast cell–derived tumor necrosis factor α (TNF-α) plays a critical role in a number of inflammatory responses by recruiting inflammatory leukocytes. In this paper, we investigated the regulatory role of interleukin 4 (IL-4) in TNF-α production in mast cells. IL-4 inhibited immunoglobulin E–induced TNF-α production and neutrophil recruitment in the peritoneal cavity in wild-type mice but not in signal transducers and activators of transcription 6 (Stat6)–deficient mice. IL-4 also inhibited TNF-α production in cultured mast cells by a Stat6-dependent mechani

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19

Liu, Kun, Hai-ling Luo, Zhao-yun Zuo та ін. "Regulation of sheep α-TTP by dietary vitamin E and preparation of monoclonal antibody for sheep α-TTP". Gene 540, № 1 (2014): 110–16. http://dx.doi.org/10.1016/j.gene.2014.02.048.

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20

Zhu, Wei, Maria A. Brauchle, Franco Di Padova, et al. "Gene suppression by tristetraprolin and release by the p38 pathway." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 2 (2001): L499—L508. http://dx.doi.org/10.1152/ajplung.2001.281.2.l499.

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Tristetraprolin (TTP) is a zinc finger protein that has been implicated in the control of tumor necrosis factor (TNF) mRNA stability. We show here that TTP protein has a suppressive effect on promoter elements from TNF-α and interleukin-8 and that lipopolysaccharide (LPS) stimulation can release this suppression. The release in LPS-stimulated cells was found to be primarily mediated by the p38 pathway because activation of p38 is sufficient to remove the suppressive effect of TTP. Indeed, TTP seems to be a direct substrate of p38 in vivo since it is an excellent substrate of p38 in vitro, and

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21

Liu, Jianguo, Jiawei Wei, Ning Huan, et al. "Mycobacterium tuberculosis induces immune evasion in macrophages through RNA-binding protein tristetraprolin." Journal of Immunology 210, no. 1_Supplement (2023): 160.16. http://dx.doi.org/10.4049/jimmunol.210.supp.160.16.

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Abstract Immune evasion of Mycobacterium tuberculosis (Mtb) facilitates intracellular bacterial growth. The mechanisms of immune evasion, however, are still not fully understood. In this study, we reveal that tristetraprolin (TTP), one of the best characterized RNA-binding proteins controlling stability of the target mRNAs, mediates innate immune evasion of mycobacteria. We found that TTP knockout mice displayed reduced bacterial burden in the early stage after Mtb aerosol challenge. Macrophages deficient in TTP also showed an inhibition in mycobacterial growth. Live mycobacteria induced TTP p

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Jalonen, Ulla, Riina Nieminen, Katriina Vuolteenaho, Hannu Kankaanranta та Eeva Moilanen. "Down-Regulation of Tristetraprolin Expression Results in Enhanced IL-12 and MIP-2 Production and Reduced MIP-3αSynthesis in Activated Macrophages". Mediators of Inflammation 2006 (2006): 1–8. http://dx.doi.org/10.1155/mi/2006/40691.

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In inflammation, the post-transcriptional regulation of transiently expressed genes provides a potential therapeutic target. Tristetraprolin (TTP) is of the factors regulating decay of cytokine mRNAs. The aim of the present study was to identify cytokines whose expression is regulated by TTP. We established a TTP knock-down cell line by expressing shRNA against TTP (shTTP cell line). A cytokine antibody array was used to measure cytokine production in macrophages exposed to lipopolysaccharide (LPS). Cytokines IL-6, IL-12, TNF-α, and MIP-2 (a homologue to human IL-8) were expressed at higher le

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Tao, Xianzun, and Guangxia Gao. "Tristetraprolin Recruits Eukaryotic Initiation Factor 4E2 To Repress Translation of AU-Rich Element-Containing mRNAs." Molecular and Cellular Biology 35, no. 22 (2015): 3921–32. http://dx.doi.org/10.1128/mcb.00845-15.

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Tristetraprolin (TTP) regulates the expression of AU-rich element-containing mRNAs through promoting the degradation and repressing the translation of target mRNA. While the mechanism for promoting target mRNA degradation has been extensively studied, the mechanism underlying translational repression is not well established. Here, we show that TTP recruits eukaryotic initiation factor 4E2 (eIF4E2) to repress target mRNA translation. TTP interacted with eIF4E2 but not with eIF4E. Overexpression of eIF4E2 enhanced TTP-mediated translational repression, and downregulation of endogenous eIF4E2 or

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Prabhala, Pavan, Kristin Bunge, Md Mostafizur Rahman, Qi Ge, Andrew R. Clark, and Alaina J. Ammit. "Temporal regulation of cytokine mRNA expression by tristetraprolin: dynamic control by p38 MAPK and MKP-1." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 9 (2015): L973—L980. http://dx.doi.org/10.1152/ajplung.00219.2014.

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Cytokines drive many inflammatory diseases, including asthma. Understanding the molecular mechanisms responsible for cytokine secretion will allow us to develop novel strategies to repress inflammation in the future. Harnessing the power of endogenous anti-inflammatory proteins is one such strategy. In this study, we investigate the p38 MAPK-mediated regulatory interaction of two anti-inflammatory proteins, mitogen-activated protein kinase phosphatase 1 (MKP-1) and tristetraprolin (TTP), in the context of asthmatic inflammation. Using primary cultures of airway smooth muscle cells in vitro, we

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Lee, Yuan-Chin, Jing-Ting Chiou, Liang-Jun Wang, Yi-Jun Shi, Ying-Jung Chen та Long-Sen Chang. "Carboxyl Group-Modified Myoglobin Induces TNF-α-Mediated Apoptosis in Leukemia Cells". Pharmaceuticals 15, № 9 (2022): 1066. http://dx.doi.org/10.3390/ph15091066.

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Previous studies have shown that chemical modification may increase the activity of proteins or confer novel activity to proteins. Some studies have indicated that myoglobin (Mb) is cytotoxic; however, the underlying mechanisms remain unclear. In this study, we investigated whether chemical modification of the carboxyl group by semicarbazide could promote the Mb cytotoxicity in human leukemia U937 cells and the underlying mechanism of semicarbazide-modified myoglobin (SEM-Mb)-induced U937 cell death. The semicarbazide-modified Mb (SEM-Mb) induced U937 cell apoptosis via the production of cleav

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Chen, Yingqing, Jeongmin Park, Yeonsoo Joe та ін. "Pterostilbene 4′-β-Glucoside Protects against DSS-Induced Colitis via Induction of Tristetraprolin". Oxidative Medicine and Cellular Longevity 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/9427583.

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Pterostilbene, a dimethyl ester analog of resveratrol, has anti-inflammatory and antioxidative effects and alters cell proliferation. Tristetraprolin (TTP) promotes the degradation of proinflammatory mediators via binding to adenosine and uridine- (AU-) rich elements (ARE) located in the 3′-untranslated regions of mRNAs. Here, we utilized pterostilbene 4′-β-glucoside (4-PG), a compound derived from pterostilbene, to investigate whether it has anti-inflammatory effects on dextran sulfate sodium- (DSS-) induced colitis via TTP enhancement. TTP expression was increased in 4-PG dose- and time-depe

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Blomberg, Bonnie, Maria Romero, Alain Diaz, Ana Landin, Richard Riley та Daniela Frasca. "Mechanisms for TNF-α-mediated down-regulation of murine B cell responses with age (113.13)". Journal of Immunology 186, № 1_Supplement (2011): 113.13. http://dx.doi.org/10.4049/jimmunol.186.supp.113.13.

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Abstract In humans, inflammatory cytokines increase with age and have deleterious effects on the immune, cardiac and nervous systems. In this study, we investigated whether this increase also occurs in mice and whether B cells contribute to this by secreting pro-inflammatory cytokines, such as TNF-α. Our hypothesis is that the following changes occur in B cells from old mice: ↑TNF-α → ↑TTP → ↓E47 and TNF-α → ↓AID, CSR Briefly, the transcription factor E47 and AID (activation-induced cytidine deaminase), both crucial for class switch recombination, are decreased with age. We show that unstimula

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Al-Daghri, Nasser M., Albatul Y. A. Al-Shuwaie, Amani Alghamdi, et al. "Tristetraprolin, Inflammation, and Metabolic Syndrome in Arab Adults: A Case Control Study." Biology 10, no. 6 (2021): 550. http://dx.doi.org/10.3390/biology10060550.

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Tristetraprolin (TTP) is an mRNA binding protein suggested to have a substantial role in regulating the mRNA expression of numerous inflammatory factors, but data on TTP and its association with metabolic syndrome (MetS), a chronic low-grade inflammatory disorder, are scarce. We hypothesize that TTP may modulate MetS and its components. A total of 200 Saudi adults (aged 38.6 ± 8.3 years) were included in this cross-sectional study. Anthropometrics data were collected and fasting blood glucose taken for the assessment of glycemic, lipids and inflammatory markers using commercially available ass

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Kang, Jong Soon, Ki Hwan Park, Sang-Bae Han та ін. "Hypothemycin inhibits tumor necrosis factor-α production by post-transcriptional regulation in lipopolysaccharide-stimulated RAW 264.7 cells (P5046)". Journal of Immunology 190, № 1_Supplement (2013): 180.6. http://dx.doi.org/10.4049/jimmunol.190.supp.180.6.

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Abstract Tumor necrosis factor-α (TNF-α) is a major inflammatory cytokine produced by activated macrophages and lymphocytes and involved in the development of many inflammatory diseases. Preventing the production or action of TNF-α is considered as a promising therapeutic strategy for various inflammatory diseases. The resorcylic acid lactone hypothemycin has been shown to exert an antitumor activity. In this study, we studied the inhibitory effects of hypothemycin on TNF-α production and underlying mechamisms. Hypothemycin dose-dependently suppressed lipopolysaccharide (LPS)-induced TNF-α sec

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Blackshear, P. J. "Tristetraprolin and other CCCH tandem zinc-finger proteins in the regulation of mRNA turnover." Biochemical Society Transactions 30, no. 6 (2002): 945–52. http://dx.doi.org/10.1042/bst0300945.

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The tristetraprolin (TTP) family of CCCH tandem zinc-finger proteins is composed of three known members in mammals, with a fourth member recently identified in frogs and fish. Although TTP was first cloned more than 10 years ago as a growth factor-induced gene, a physiological function for the protein has been discovered only within the last few years. TTP is now known to bind to so-called class II AU-rich elements within the mRNAs that encode tumour necrosis factor-α and granulocyte/macrophage colony-stimulating factor. In both cases, this binding results in destabilization of the mRNA and de

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Jimenez, Joaquin J., Wenche Jy, Lucia M. Mauro, et al. "Increased Endothelial Colony-Forming Cells (ECFC) and Endothelial Microparticles (EMP) and Their Interaction in Thrombotic Thrombocytopenic Purpura (TTP)." Blood 110, no. 11 (2007): 3908. http://dx.doi.org/10.1182/blood.v110.11.3908.3908.

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Abstract BACKGROUND. Endothelial damage is a prominent feature of TTP, evidenced by elevated EMP levels during acute episodes of TTP. However, endothelial repair in TTP remains to be investigated. ECFC are key players in endothelial regeneration, and their assay in blood has been employed to monitor endothelial remodeling. We investigated circulating ECFC in TTP and their relationship with EMP. METHODS. Six patients with acquired TTP were studied. All were treated with therapeutic plasma exchange (TPE). All but one underwent complete remission (CR). The one who failed to achieve CR with TPE su

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Jimenez, Joaquin J., Wenche Jy, Lucia M. Mauro, et al. "Activation of Endothelial Cells (EC) Leads to Release of Inhibitory Endothelial Microparticles (EMP) and Decreased Intracellular ADAMTS13 Activity." Blood 108, no. 11 (2006): 1810. http://dx.doi.org/10.1182/blood.v108.11.1810.1810.

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Abstract BACKGROUND: Deficiency of the von Willebrand factor (vWF)-cleaving protease ADAMTS13 is known to be involved in the pathogenesis of idiopathic thrombotic thrombocytopenic purpura (TTP). A recent study has shown that in addition to liver, endothelial cells (EC) are a site of production of ADAMTS13 [D. Shang et al, Blood online 2006, prepub.]. Perturbation of EC has been implicated as the primary lesion in TTP and it has been demonstrated that markers of EC activation are increased in TTP. We previously documented elevated EMP positive for unusually large vWF (ULvWF) in TTP patients, an

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Steinkamp, H. M., J. D. Hathaway-Schrader, M. B. Chavez, et al. "Tristetraprolin Is Required for Alveolar Bone Homeostasis." Journal of Dental Research 97, no. 8 (2018): 946–53. http://dx.doi.org/10.1177/0022034518756889.

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Tristetraprolin (TTP) is an RNA-binding protein that targets numerous immunomodulatory mRNA transcripts for degradation. Many TTP targets are key players in the pathogenesis of periodontal bone loss, including tumor necrosis factor–α. To better understand the extent that host immune factors play during periodontal bone loss, we assessed alveolar bone levels, inflammation and osteoclast activity in periodontal tissues, and immune response in draining cervical lymph nodes in TTP-deficient and wild-type (WT) mice in an aging study. WT and TTP-deficient (knockout [KO]) mice were used for all studi

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Zorina, L. V., S. V. Simonov, S. S. Khasanov та R. P. Shibaeva. "New low-dimensional molecular conductors: α′′-(BEDO-TTF)2Cl·3H2O andθ-(BDH-TTP)2(Br0.67Cl0.33)·3H2O". Low Temperature Physics 37, № 10 (2011): 744–48. http://dx.doi.org/10.1063/1.3665894.

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Shichiri, Mototada, Nozomu Kono, Yuta Shimanaka та ін. "A Novel Role for α-Tocopherol Transfer Protein (α-TTP) in Protecting against Chloroquine Toxicity". Journal of Biological Chemistry 287, № 4 (2011): 2926–34. http://dx.doi.org/10.1074/jbc.m111.321281.

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Ait-Oudhia, Sihem, Donald E. Mager, Garin Tomaszewski, et al. "Bridging sunitinib exposure to time-to-tumor progression in hepatocellular carcinoma patients with mathematical modeling of an angiogenic biomarker." Journal of Clinical Oncology 30, no. 15_suppl (2012): e14690-e14690. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14690.

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e14690 Background: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy with 250,000 new annual cases in the US. Sunitinib (SU), an oral tyrosine kinase inhibitor, inhibits tumor cell proliferation, selectively binds to the angiogenesis biomarker (VEGFR2), and is metabolized to an equipotent metabolite (SU12662). The objective of this study is to utilize mathematical modeling to bridge drug exposure and VEGFR2 dynamics to tumor growth inhibition (TGI) and time-to-tumor progression (TTP). Methods: Plasma concentrations of SU, SU12662, and VEGFR2, and tumor growth and TTP m

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Clemente, Alfredo, Guerino Selva, Michael Berks, et al. "Comparison of Early Contrast Enhancement Models in Ultrafast Dynamic Contrast-Enhanced Magnetic Resonance Imaging of Prostate Cancer." Diagnostics 14, no. 9 (2024): 870. http://dx.doi.org/10.3390/diagnostics14090870.

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Tofts models have failed to produce reliable quantitative markers for prostate cancer. We examined the differences between prostate zones and lesion PI-RADS categories and grade group (GG) using regions of interest drawn in tumor and normal-appearing tissue for a two-compartment uptake (2CU) model (including plasma volume (vp), plasma flow (Fp), permeability surface area product (PS), plasma mean transit time (MTTp), capillary transit time (Tc), extraction fraction (E), and transfer constant (Ktrans)) and exponential (amplitude (A), arrival time (t0), and enhancement rate (α)), sigmoidal (ampl

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Horiguchi, Masakuni, Makoto Arita, Daisy E. Kaempf-Rotzoll, Masafumi Tsujimoto, Keizo Inoue та Hiroyuki Arai. "pH-dependent translocation of α-tocopherol transfer protein (α-TTP) between hepatic cytosol and late endosomes". Genes to Cells 8, № 10 (2003): 789–800. http://dx.doi.org/10.1046/j.1365-2443.2003.00676.x.

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Rodriguez Freixinos, Victor, Fiorella Ruiz-Pace, Lorena Fariñas-Madrid, et al. "Impact of genomic heterogeneity on PI3K/AKT/mTOR inhibitors (PAMi) efficacy in gynecologic cancer (GYN) patients (pts)." Journal of Clinical Oncology 35, no. 15_suppl (2017): 5569. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.5569.

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5569 Background: Aberrant PI3K/AKT/mTOR activation is common in GYN. Predictive biomarkers to PAMi in GYN have yet to be identified. Methods: Advanced GYN pts with available genomic data, treated with PAMi in phase I/II clinical trials were selected. Mutation (mut) allele fractions (MAFs) were corrected for tumor purity and defined as clonal (cl) (≥ 0.4) or subclonal (scl) ( < 0.4). PAMi efficacy: (i) time to progression (TTP); (ii) clinical benefit rate (CBR: complete/partial response or stable disease > 4 months [m]); and (iii) ratio TTP on PAMi/ TTP on non-standard chemotherapy pre- o

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Kushch, N. D., A. V. Kazakova, L. I. Buravov та ін. "The first BDH-TTP radical cation salts with mercuric counterions, κ-(BDH-TTP)4[Hg(SCN)4]·C6H5NO2 and α′-(BDH-TTP)6[Hg(SCN)3][Hg(SCN)4]". Synthetic Metals 155, № 3 (2005): 588–94. http://dx.doi.org/10.1016/j.synthmet.2005.09.038.

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Yeh, Shu-Hui, Wen-Kuang Hsu, Zi-Qing Chang, et al. "Purification and Characterization of Fractions Containing Polysaccharides from Talinum triangulare and Their Immunomodulatory Effects." Processes 9, no. 4 (2021): 709. http://dx.doi.org/10.3390/pr9040709.

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Previous studies identified that extracts of Talinum triangulare rich in flavonoids and phenolic acids showed antioxidative and immunomodulatory activities. In this study, the L9 orthogonal array was used to determine the optimal extraction conditions for water-extracted polysaccharides of T. triangulare (TTP) by hot reflux extraction and ultrasonic assisted extraction (UAE) methods. Results showed that while both extraction methods obtained a maximum polysaccharide yield of 3.1%, the optimal conditions for obtaining TTP was by UAE method. TTP was separated into large (LTTP) and small (STTP) m

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Sun, Lei, Georg Stoecklin, Susan Van Way та ін. "Tristetraprolin (TTP)-14-3-3 Complex Formation Protects TTP from Dephosphorylation by Protein Phosphatase 2a and Stabilizes Tumor Necrosis Factor-α mRNA". Journal of Biological Chemistry 282, № 6 (2007): 3766–77. http://dx.doi.org/10.1074/jbc.m607347200.

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Taguchi, Yoshitomo, Mari Komatsu-Tanaka, Norie Hirose, Yurie Kaji та Kazuhiro Saeki. "Molecular Cloning and Expression Analysis of Bovine Alpha-tocopherol Transfer Protein (α-TTP)". Annual Research & Review in Biology 12, № 5 (2017): 1–7. http://dx.doi.org/10.9734/arrb/2017/33400.

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Helbling, Rachel E., Walter Aeschimann, Fabio Simona, Achim Stocker та Michele Cascella. "Engineering Tocopherol Selectivity in α-TTP: A Combined In Vitro/In Silico Study". PLoS ONE 7, № 11 (2012): e49195. http://dx.doi.org/10.1371/journal.pone.0049195.

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Ademokun, Alexander, and Martin Turner. "Regulation of B-cell differentiation by microRNAs and RNA-binding proteins." Biochemical Society Transactions 36, no. 6 (2008): 1191–93. http://dx.doi.org/10.1042/bst0361191.

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Post-transcriptional control of gene expression is an important mechanism for maintaining cellular homoeostasis and regulating the immune response to infection. It allows control of mRNA abundance, translation and localization. Mechanisms for post-transcriptional control involve RNA-binding proteins and miRNAs (microRNAs). The TTP(tristetraprolin) family of proteins recognize and bind AU-rich elements. Deletion of TTP led to a systemic autoimmune syndrome with excess circulating TNFα (tumour necrosis factor α) and GM-CSF (granulocyte/macrophage colony-stimulating factor) due to aberrantly stab

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Bao, Jialing, Khalil Bdeir, Don L. Siegel, Douglas B. Cines, and X. Long Zheng. "Inhibition of ADAMTS13 Activity By Human Neutrophil Peptide 1 (HNP-1): Potential Link Between Inflammation, Onset of Thrombotic Thrombocytopenic Purpura, and Other Thrombosis." Blood 124, no. 21 (2014): 599. http://dx.doi.org/10.1182/blood.v124.21.599.599.

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Abstract Thrombotic thrombocytopenic purpura (TTP) is a potentially fatal syndrome associated with severe deficiency of plasma ADAMTS13 activity resulting from either mutations or autoantibodies. However, patients with severe ADAMTS13 deficiency do not always develop TTP. Rather, a trigger, such as infection or inflammation, often precedes the onset of the TTP syndrome. We hypothesized that antimicrobial human neutrophil peptides 1-3 (HNPα1-3) or α-defensins, the most abundant proteins in the granules of neutrophils, which are released at site of inflammation, activate platelets, and inhibit f

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Goy, Andre, Steven H. Bernstein, Alice McDonald, et al. "Immunohistochemical Analyses for Potential Biomarkers of Bortezomib Activity in Mantle Cell Lymphoma from the PINNACLE Phase 2 Trial." Blood 110, no. 11 (2007): 2573. http://dx.doi.org/10.1182/blood.v110.11.2573.2573.

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Abstract Background: Mantle cell lymphoma (MCL) is an aggressive NHL subtype that remains incurable in most cases with conventional chemotherapy. However, individual patient survival can vary considerably, and studies have identified potential markers of prognostic subgroups, including Ki-67 and the cyclin-dependent kinase (CDK) inhibitor p27. Genomic studies further highlight tumor proliferation status as the major driver of differential prognosis in MCL (Rosenwald et al, Cancer Cell 2003). Such studies were conducted prior to the introduction of bortezomib, a first-in-class proteasome inhibi

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Wan, Yue-Meng, Yu-Hua Li, Zhi-Yuan Xu, et al. "The Effect of Transarterial Chemoembolization in Combination With Kang’ai Injection on Patients With Intermediate Stage Hepatocellular Carcinoma: A Prospective Study." Integrative Cancer Therapies 17, no. 2 (2017): 477–85. http://dx.doi.org/10.1177/1534735417734913.

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Background: The outcome of patients with intermediate stage hepatocellular carcinoma (HCC) treated by transarterial chemoembolization (TACE) remains poor. Search for a more effective therapy is still necessary. Objective: This study aimed to investigate the effect of combining TACE with Kang’ai (KA) injection for treating patients with intermediate stage HCC. Methods: A total of 89 patients with intermediate stage HCC were enrolled and divided into TACE +KA group (n = 48) receiving repeated TACE plus KA injection, and TACE group (n = 41) receiving repeated TACE alone. All patients were prospec

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Zhang, Wen Xiao, Varsha Thakur, Andrei Lomize та ін. "The Contribution of Surface Residues to Membrane Binding and Ligand Transfer by the α-Tocopherol Transfer Protein (α-TTP)". Journal of Molecular Biology 405, № 4 (2011): 972–88. http://dx.doi.org/10.1016/j.jmb.2010.11.028.

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Sze, Kit-Ling, Wing-Yee Lui та Will M. Lee. "Post-transcriptional regulation of CLMP mRNA is controlled by tristetraprolin in response to TNFα via c-Jun N-terminal kinase signalling". Biochemical Journal 410, № 3 (2008): 575–83. http://dx.doi.org/10.1042/bj20070901.

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During spermatogenesis, extensive restructuring of blood–testis barrier takes place to facilitate the migration of preleptotene/leptotene spermatocytes from the basal to the adluminal compartment in the seminiferous epithelium. However, the biochemical mechanisms involved in this event remain elusive. Recent studies have shown that pro-inflammatory cytokine TNFα (tumour necrosis factor α) plays a crucial role in this event by inhibiting the expression of tight junction proteins in Sertoli cells. In the present study, we sought to examine the detailed mechanism on how TNFα affects the expressio

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