Статті в журналах: "TAB2"

1

CHEUNG, Peter C. F., Angel R. NEBREDA, and Philip COHEN. "TAB3, a new binding partner of the protein kinase TAK1." Biochemical Journal 378, no. 1 (February 15, 2004): 27–34. http://dx.doi.org/10.1042/bj20031794.

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We have identified a new binding partner of the TGFβ (transforming growth factor-β)-activated protein kinase (TAK1), termed TAB3 (TAK1-binding protein-3), which shares 48% amino acid sequence identity with TAB2. Our results indicate that two distinct TAK1 complexes are present in cells. One comprises TAK1 complexed with TAB1 and TAB2, and the other TAK1 complexed with TAB1 and TAB3. Both complexes are activated in response to tumour necrosis factor-α or interleukin-1 in human epithelial KB cells or bacterial lipopolysaccharide in RAW264.7 macrophages, and are subject to feedback control by stress-activated protein kinase 2a (SAPK2a; also called p38α). The electrophoretic mobility of TAB2 and TAB3 decreases in response to these agonists or osmotic shock, and is reversed by treatment with protein phosphatase-1. The decrease in mobility of TAB3 is prevented if the cells are incubated with SB 203580 before stimulation, but treatment with SB 203580 produces forms of TAB2 with a mobility intermediate between that observed for TAB2 in unstimulated and stimulated cells. Similar results were obtained in embryonic fibroblasts from mice deficient in SAPK2a/p38α. Our results indicate that TAB3 is phosphorylated via the SAPK2a/p38α pathway, whereas TAB2 is phosphorylated at two or more sites by both an SAPK2a/p38α-dependent and an SB 203580-independent kinase. The SAPK2a/p38α-mediated phosphorylation of TAB2 and TAB3 may contribute to the SAPK2a/p38α-mediated feedback control of TAK1 activity that also involves the phosphorylation of TAB1. We also show that the agonist-induced activation of TAK1 complexes requires the phosphorylation of the TAK1 catalytic subunit at a serine/threonine residue(s).

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2

Zhang, Jiazhen, Thomas Macartney, Mark Peggie, and Philip Cohen. "Interleukin-1 and TRAF6-dependent activation of TAK1 in the absence of TAB2 and TAB3." Biochemical Journal 474, no. 13 (June 26, 2017): 2235–48. http://dx.doi.org/10.1042/bcj20170288.

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Interleukin-1 (IL-1) signaling induces the formation of Lys63-linked ubiquitin (K63-Ub) chains, which are thought to activate the ‘master’ protein kinase TGFβ-activated kinase 1 (TAK1) by interacting with its TAK1-binding 2 (TAB2) and TAB3 subunits. Here, we report that IL-1β can also activate the TAB1–TAK1 heterodimer present in TAB2/TAB3 double knockout (DKO) IL-1 receptor-expressing cells. The IL-1β-dependent activation of the TAB1–TAK1 heterodimer in TAB2/3 DKO cells is required for the expression and E3 ligase activity of tumor necrosis factor receptor-associated factor 6 (TRAF6) and is reduced by the small interfering RNA (siRNA) knockdown of ubiquitin conjugating 13 (Ubc13), an E2-conjugating enzyme that directs the formation of K63-Ub chains. IL-1β signaling was restored to TAB1/2/3 triple KO cells by the re-expression of either TAB1 or TAB2, but not by an ubiquitin binding-defective mutant of TAB2. We conclude that IL-1β can induce the activation of TAK1 in two ways, only one of which requires the binding of K63-Ub chains to TAB2/3. The early IL-1β-stimulated, TAK1-dependent activation of p38α mitogen-activated protein (MAP) kinase and the canonical IκB kinase (IKK) complex, as well as the NF-κB-dependent transcription of immediate early genes, was similar in TAB2/3 DKO cells and TAB2/3-expressing cells. However, in contrast with TAB2/3-expressing cells, IL-1β signaling was transient in TAB2/3 DKO cells, and the activation of c-Jun N-terminal kinase 1 (JNK1), JNK2 and p38γ was greatly reduced at all times. These observations indicate a role for TAB2/3 in directing the TAK1-dependent activation of MAP kinase kinases that switch on JNK1/2 and p38γ MAP kinases. These observations and the transient activation of the TAB1–TAK1 heterodimer may explain why IL-1β-dependent IL-8 mRNA formation was abolished in TAB2/3 DKO cells.

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3

Mendoza, Heidi, David G. Campbell, Kerry Burness, James Hastie, Natalia Ronkina, Jae-Hyuck Shim, J. Simon C. Arthur, et al. "Roles for TAB1 in regulating the IL-1-dependent phosphorylation of the TAB3 regulatory subunit and activity of the TAK1 complex." Biochemical Journal 409, no. 3 (January 15, 2008): 711–22. http://dx.doi.org/10.1042/bj20071149.

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The protein kinase TAK1 (transforming growth factor-β-activated kinase 1), which has been implicated in the activation of MAPK (mitogen-activated protein kinase) cascades and the production of inflammatory mediators by LPS (lipopolysaccharide), IL-1 (interleukin 1) and TNF (tumour necrosis factor), comprises the catalytic subunit complexed to the regulatory subunits, termed TAB (TAK1-binding subunit) 1 and either TAB2 or TAB3. We have previously identified a feedback-control mechanism by which p38α MAPK down-regulates TAK1 and showed that p38α MAPK phosphorylates TAB1 at Ser423 and Thr431. In the present study, we identified two IL-1-stimulated phosphorylation sites on TAB2 (Ser372 and Ser524) and three on TAB3 (Ser60, Thr404 and Ser506) in human IL-1R cells [HEK-293 (human embryonic kidney) cells that stably express the IL-1 receptor] and MEFs (mouse embryonic fibroblasts). Ser372 and Ser524 of TAB2 are not phosphorylated by pathways dependent on p38α/β MAPKs, ERK1/2 (extracellular-signal-regulated kinase 1/2) and JNK1/2 (c-Jun N-terminal kinase 1/2). In contrast, Ser60 and Thr404 of TAB3 appear to be phosphorylated directly by p38α MAPK, whereas Ser506 is phosphorylated by MAPKAP-K2/MAPKAP-K3 (MAPK-activated protein kinase 2 and 3), which are protein kinases activated by p38α MAPK. Studies using TAB1−/− MEFs indicate important roles for TAB1 in recruiting p38α MAPK to the TAK1 complex for the phosphorylation of TAB3 at Ser60 and Thr404 and in inhibiting the dephosphorylation of TAB3 at Ser506. TAB1 is also required to induce TAK1 catalytic activity, since neither IL-1 nor TNFα was able to stimulate detectable TAK1 activity in TAB1−/− MEFs. Surprisingly, the IL-1 and TNFα-stimulated activation of MAPK cascades and IκB (inhibitor of nuclear factor κB) kinases were similar in TAB1−/−, MEKK3−/− [MAPK/ERK (extracellular-signal-regulated kinase) kinase kinase 3] and wild-type MEFs, suggesting that another MAP3K (MAPK kinase kinase) may mediate the IL-1/TNFα-induced activation of these signalling pathways in TAB1−/− and MEKK3−/− MEFs.

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4

Grimsey, Neil J., Berenice Aguilar, Thomas H. Smith, Phillip Le, Amanda L. Soohoo, Manojkumar A. Puthenveedu, Victor Nizet, and JoAnn Trejo. "Ubiquitin plays an atypical role in GPCR-induced p38 MAP kinase activation on endosomes." Journal of Cell Biology 210, no. 7 (September 21, 2015): 1117–31. http://dx.doi.org/10.1083/jcb.201504007.

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Protease-activated receptor 1 (PAR1) is a G protein–coupled receptor (GPCR) for thrombin and promotes inflammatory responses through multiple pathways including p38 mitogen-activated protein kinase signaling. The mechanisms that govern PAR1-induced p38 activation remain unclear. Here, we define an atypical ubiquitin-dependent pathway for p38 activation used by PAR1 that regulates endothelial barrier permeability. Activated PAR1 K63-linked ubiquitination is mediated by the NEDD4-2 E3 ubiquitin ligase and initiated recruitment of transforming growth factor-β–activated protein kinase-1 binding protein-2 (TAB2). The ubiquitin-binding domain of TAB2 was essential for recruitment to PAR1-containing endosomes. TAB2 associated with TAB1, which induced p38 activation independent of MKK3 and MKK6. The P2Y1 purinergic GPCR also stimulated p38 activation via NEDD4-2–mediated ubiquitination and TAB1–TAB2. TAB1–TAB2-dependent p38 activation was critical for PAR1-promoted endothelial barrier permeability in vitro, and p38 signaling was required for PAR1-induced vascular leakage in vivo. These studies define an atypical ubiquitin-mediated signaling pathway used by a subset of GPCRs that regulates endosomal p38 signaling and endothelial barrier disruption.

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5

Morioka, Sho, Maiko Inagaki, Yoshihiro Komatsu, Yuji Mishina, Kunihiro Matsumoto, and Jun Ninomiya-Tsuji. "TAK1 kinase signaling regulates embryonic angiogenesis by modulating endothelial cell survival and migration." Blood 120, no. 18 (November 1, 2012): 3846–57. http://dx.doi.org/10.1182/blood-2012-03-416198.

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Abstract TGF-β activated kinase 1 (TAK1) is a mediator of various cytokine signaling pathways. Germline deficiency of Tak1 causes multiple abnormalities, including dilated blood vessels at midgestation. However, the mechanisms by which TAK1 regulates vessel formation have not been elucidated. TAK1 binding proteins 1 and 2 (TAB1 and TAB2) are activators of TAK1, but their roles in embryonic TAK1 signaling have not been determined. In the present study, we characterized mouse embryos harboring endothelial-specific deletions of Tak1, Tab1, or Tab2 and found that endothelial TAK1 and TAB2, but not TAB1, were critically involved in vascular formation. TAK1 deficiency in endothelial cells caused increased cell death and vessel regression at embryonic day 10.5 (E10.5). Deletion of TNF signaling largely rescued endothelial cell death in TAK1-deficient embryos at E10.5. However, embryos deficient in both TAK1 and TNF signaling still exhibited dilated capillary networks at E12.5. TAB2 deficiency caused reduced TAK1 activity, resulting in abnormal capillary blood vessels, similar to the compound deficiency of TAK1 and TNF signaling. Ablation of either TAK1 or TAB2 impaired cell migration and tube formation. Our results show that endothelial TAK1 signaling is important for 2 biologic processes in angiogenesis: inhibiting TNF-dependent endothelial cell death and promoting TNF-independent angiogenic cell migration.

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6

Sanjo, Hideki, Kiyoshi Takeda, Tohru Tsujimura, Jun Ninomiya-Tsuji, Kunihiro Matsumoto, and Shizuo Akira. "TAB2 Is Essential for Prevention of Apoptosis in Fetal Liver but Not for Interleukin-1 Signaling." Molecular and Cellular Biology 23, no. 4 (February 15, 2003): 1231–38. http://dx.doi.org/10.1128/mcb.23.4.1231-1238.2003.

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ABSTRACT The proinflammatory cytokine interleukin-1 (IL-1) transmits a signal via several critical cytoplasmic proteins such as MyD88, IRAKs and TRAF6. Recently, serine/threonine kinase TAK1 and TAK1 binding protein 1 and 2 (TAB1/2) have been identified as molecules involved in IL-1-induced TRAF6-mediated activation of AP-1 and NF-κB via mitogen-activated protein (MAP) kinases and IκB kinases, respectively. However, their physiological functions remain to be clarified. To elucidate their roles in vivo, we generated TAB2-deficient mice. The TAB2 deficiency was embryonic lethal due to liver degeneration and apoptosis. This phenotype was similar to that of NF-κB p65-, IKKβ-, and NEMO/IKKγ-deficient mice. However, the IL-1-induced activation of NF-κB and MAP kinases was not impaired in TAB2-deficient embryonic fibroblasts. These findings demonstrate that TAB2 is essential for embryonic development through prevention of liver apoptosis but not for the IL-1 receptor-mediated signaling pathway.

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7

Makarova, O. V., L. P. Polyakova, E. G. Polyakov, A. A. Shevyryov, and A. V. Arakcheeva. "Phase composition of cathodic deposits synthesized in flinak-k2taf7-kbf4 melt." Journal of Mining and Metallurgy, Section B: Metallurgy 39, no. 1-2 (2003): 261–67. http://dx.doi.org/10.2298/jmmb0302261m.

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The phase composition of cathodic deposits synthesized from FLINAK-K2TaF7-KBF4 melt has been studied by the X-ray diffraction method. It is shown that boron content in the electrodeposit grows as the cathodic potential is increased from peak R1 to peak R4 in the voltammogram. The scheme of changes in the phase composition depending on the increasing current density is given as follows: {?-Ta + Ta2B}R1 ? {?-Ta + (Ta3B4 TaB)}R2 ? {TaB2}R3 ? {TaB2 + B}R4.

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8

Criollo, Alfredo, Mireia Niso-Santano, Shoaib Ahmad Malik, Mickael Michaud, Eugenia Morselli, Guillermo Mariño, Sylvie Lachkar, et al. "Inhibition of autophagy by TAB2 and TAB3." EMBO Journal 30, no. 24 (November 11, 2011): 4908–20. http://dx.doi.org/10.1038/emboj.2011.413.

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9

Jiang, Zhengfan, Jun Ninomiya-Tsuji, Youcun Qian, Kunihiro Matsumoto, and Xiaoxia Li. "Interleukin-1 (IL-1) Receptor-Associated Kinase-Dependent IL-1-Induced Signaling Complexes Phosphorylate TAK1 and TAB2 at the Plasma Membrane and Activate TAK1 in the Cytosol." Molecular and Cellular Biology 22, no. 20 (October 15, 2002): 7158–67. http://dx.doi.org/10.1128/mcb.22.20.7158-7167.2002.

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ABSTRACT Interleukin-1 (IL-1) receptor-associated kinase (IRAK) plays an important role in the sequential formation and activation of IL-1-induced signaling complexes. Previous studies showed that IRAK is recruited to the IL-1-receptor complex, where it is hyperphosphorylated. We now find that the phosphorylated IRAK in turn recruits TRAF6 to the receptor complex (complex I), which differs from the previous concept that IRAK interacts with TRAF6 after it leaves the receptor. IRAK then brings TRAF6 to TAK1, TAB1, and TAB2, which are preassociated on the membrane before stimulation to form the membrane-associated complex II. The formation of complex II leads to the phosphorylation of TAK1 and TAB2 on the membrane by an unknown kinase, followed by the dissociation of TRAF6-TAK1-TAB1-TAB2 (complex III) from IRAK and consequent translocation of complex III to the cytosol. The formation of complex III and its interaction with additional cytosolic factors lead to the activation of TAK1, resulting in NF-κB and JNK activation. Phosphorylated IRAK remains on the membrane and eventually is ubiquitinated and degraded. Taken together, the new data reveal that IRAK plays a critical role in mediating the association and dissociation of IL-1-induced signaling complexes, functioning as an organizer and transporter in IL-1-dependent signaling.

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10

Lei, X., N. Han, X. Xiao, Q. Jin, B. He, and J. Wang. "Enterovirus 71 3C Inhibits Cytokine Expression through Cleavage of the TAK1/TAB1/TAB2/TAB3 Complex." Journal of Virology 88, no. 17 (June 18, 2014): 9830–41. http://dx.doi.org/10.1128/jvi.01425-14.

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11

Liu, Huijuan, Hui Zhang, Haidong Fan, Su Tang, and Junquan Weng. "TAB2 Promotes the Biological Functions of Head and Neck Squamous Cell Carcinoma Cells via EMT and PI3K Pathway." Disease Markers 2022 (August 8, 2022): 1–10. http://dx.doi.org/10.1155/2022/1217918.

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Background. Transforming growth factor β1-activated kinase 1 binding protein 2 (TAB2) mediates a variety of biological processes through activated nuclear factor κ-light-chain-enhancer of activated B cell (NF-κB) signaling pathways. TAB2 has been reported to be upregulated in a variety of tumors. However, little is known about its potential role in oral squamous cell carcinoma (OSCC). Material and Methods. Patients’ clinicopathological and transcription data were obtained from The Cancer Genome Atlas (TCGA) database. Immunohistochemistry staining was used to determine TAB2 expression in OSCC tissues (IHC). The expression of TAB2 in OSCC cell lines was detected by western blotting. The CCK-8 test and flow cytometry assay were utilized to evaluate cell proliferation, apoptosis, and cell cycle in OSCC cell lines. Enrichment analysis and identification of predicted signaling pathways were performed by Gene Ontology and KEGG analysis. Finally, the expression of downstream signal molecules was performed using western blotting to validate the mechanism investigations. Results. TAB2 expression level was aberrantly upregulated in OSCC patients. TAB2 expression was shown to be inversely associated to prognosis. The phenotypic of OSCC cells was considerably impacted by TAB2. OSCC cells with deleted TAB2 exhibit decreased proliferation and increased apoptosis. Additionally, OSCC progression is aided by TAB2 overexpression. Further mechanism studies showed that TAB2 could regulate the progression of OSCC by mediating the upregulation of EMT and PI3K-AKT signaling pathways. Conclusion. This study sheds light on the carcinogenic role of TAB2 in OSCC and provides a potential therapeutic strategy.

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12

Besse, Arnaud, Betty Lamothe, Alejandro D. Campos, William K. Webster, Upendra Maddineni, Su-Chang Lin, Hao Wu, and Bryant G. Darnay. "TAK1-dependent Signaling Requires Functional Interaction with TAB2/TAB3." Journal of Biological Chemistry 282, no. 6 (February 2007): 3918–28. http://dx.doi.org/10.1074/jbc.m608867200.

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13

Xia, Qian, Gaofeng Zhan, Meng Mao, Yin Zhao, and Xing Li. "TRIM45 causes neuronal damage by aggravating microglia-mediated neuroinflammation upon cerebral ischemia and reperfusion injury." Experimental & Molecular Medicine 54, no. 2 (February 2022): 180–93. http://dx.doi.org/10.1038/s12276-022-00734-y.

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AbstractExcessive and unresolved neuroinflammation is a key component of the pathological cascade in brain injuries such as ischemic stroke. Tripartite motif-containing 45 (TRIM45) is a ubiquitin E3 ligase involved in various critical biological processes. However, the role of TRIM45 in cerebral ischemia remains unknown. Here, we found that the TRIM45 protein was highly expressed in the peri-infarct areas of mice subjected to cerebral ischemia and reperfusion injury induced by middle cerebral artery occlusion. This study systemically evaluated the putative role of TRIM45 in the regulation of neuroinflammation during ischemic injury and the potential underlying mechanisms. We found that TRIM45 knockdown significantly decreased proinflammatory cytokine and chemokine production in primary cultured microglia challenged with oxygen-glucose deprivation and reoxygenation (OGD/R) treatment. Mechanistically, we demonstrated that TRIM45 constitutively interacted with TAB2 and consequently facilitated the Lys-63-linked polyubiquitination of TAB2, leading to the formation of the TAB1–TAK1–TAB2 complex and activation of TAK1, which was ultimately followed by activation of the nuclear factor-kappa B (NF-κB) signaling pathway. In an in vitro coculture Transwell system, downregulation of TRIM45 expression also inhibited the OGD/R-induced activation of microglia and alleviated neuronal apoptosis. More importantly, microglia-specific knockdown of TRIM45 in mice significantly reduced the infarct size, mitigated neurological deficit scores, and improved cognitive function after ischemic stroke. Taken together, our study reveals that the TRIM45–TAB2 axis is a crucial checkpoint that controls NF-κB signaling in microglia during cerebral ischemia and reperfusion injury. Therefore, targeting TRIM45 may be an attractive therapeutic strategy.

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14

Xie, Yushuai, Kun Lei, Jinquan He, and Youchuan Wei. "Molecular Characterization and Expression Analysis of TAK1, TAB1 and TAB2 of Golden Pompano (Trachinotus ovatus)." Fishes 7, no. 4 (July 18, 2022): 173. http://dx.doi.org/10.3390/fishes7040173.

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Transforming growth factor-β (TGF-β)-activated kinase 1 (TAK1), TAK1-binding protein 1 (TAB1) and TAB2 are components of the mitogen-activated protein kinase (MAPK) pathway. In this study, TAK1, TAB1 and TAB2 were characterized from golden pompano (Trachinotus ovatus), a marine fish of great economic value, and named as trTAK1, trTAB1 and trTAB2, respectively. The lengths of the cDNA sequences of the three genes were 2429 bp, 2068 bp and 4229 bp and encoded 575, 506 and 759 amino acids, respectively. The trTAK1, trTAB1 and trTAB2 genes shared high sequence identities and were well clustered with their counterparts from other fish species. Real-time qPCR analysis showed that the three genes were constitutively expressed in all the selected tissues of healthy pompano, and the expression levels of the three genes were significantly up-regulated in head kidney and spleen following Vibrio alginolyticus, lipolysaccharide (LPS) and polyinosinic polycytidylic acid (poly I:C) challenge, indicating their roles in the immune response against pathogens in golden pompano. Our results provide a basis for further study of the functions of these genes in golden pompano.

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15

Chen, Xuan, De Li, and Mangmang Chen. "MiR-493-5p alleviates lipopolysaccharide-induced inflammation in ATDC5 chondrogenic cells by targeting TAB2." Tropical Journal of Pharmaceutical Research 21, no. 11 (February 13, 2023): 2295–301. http://dx.doi.org/10.4314/tjpr.v21i11.4.

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Purpose: To investigate the effect of miR-493-5p in lipopolysaccharide (LPS) -induced ATDC5 chondrogenic cells. Methods: The MTT assay was used to determine the viability of LPS-induced ATDC5 cells. ENCORI (starbase.sysu.edu.cn/) was used to predict the target of miR-493-5p. Quantitative reverse-transcription-polymerase chain reaction (qRT-PCR) was used to determine miR-493-5p expression in ATDC5 controlled cells and cells treated with various combinations of LPS, negative control miRNA (NC), miR-493-5p mimic, TAB2 overexpression vector, and miR-493-5p inhibitor. qRT-PCR, while western blot was used to assess TAB2 mRNA and protein expression levels in control, LPS, LPS + NC, LPS + miR-493-5p mimic, and LPS + miR-493-5p inhibitor groups. The qRT-PCR and ELISA were used to evaluate TNF-α, IL-18, and IL-1β expressions in control, NC, LPS, LPS + NC, miR-493-5p mimic, and LPS + miR-493-5p mimic. Furthermore, the two techniques were also used determine LPS + miR-493-5p inhibitor, LPS + TAB2 overexpression, and LPS + TAB2 overexpression + miR-493-5p mimic groups. Results: MiR-493-5p expression was downregulated in LPS-induced ATDC5 cells (p < 0.001). Overexpression of miR-493-5p increased LPS-induced ATDC5 cell viability but decreased expression of inflammatory factors (p < 0.001). MiR-493-5p targeted and inhibited TAB2 expression in LPS-induced ATDC5 cells (p < 0.001). TAB2 overexpression reversed the suppression of TAB2 by miR-493-5p in LPS-induced ATDC5 cell injury (p < 0.001). Conclusion: MiR-493-5p alleviates LPS-induced inflammation of ATDC5 chondrogenic cells by targeting TAB2. Thus, miR-493-5p and TAB2 have potentials for use as clinical therapeutic targets for OA.

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16

Mizukami, Junko, Giichi Takaesu, Hiroyuki Akatsuka, Hiroaki Sakurai, Jun Ninomiya-Tsuji, Kunihiro Matsumoto та Naoki Sakurai. "Receptor Activator of NF-κB Ligand (RANKL) Activates TAK1 Mitogen-Activated Protein Kinase Kinase Kinase through a Signaling Complex Containing RANK, TAB2, and TRAF6". Molecular and Cellular Biology 22, № 4 (15 лютого 2002): 992–1000. http://dx.doi.org/10.1128/mcb.22.4.992-1000.2002.

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ABSTRACT The receptor activator of NF-κB (RANK) and its ligand RANKL are key molecules for differentiation and activation of osteoclasts. RANKL stimulates transcription factors AP-1 through mitogen-activated protein kinase (MAPK) activation, and NF-κB through IκB kinase (IKK) activation. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is essential for activation of these kinases. In the interleukin-1 signaling pathway, TAK1 MAPK kinase kinase (MAPKKK) mediates MAPK and IKK activation via interaction with TRAF6, and TAB2 acts as an adapter linking TAK1 and TRAF6. Here, we demonstrate that TAK1 and TAB2 participate in the RANK signaling pathway. Dominant negative forms of TAK1 and TAB2 inhibit NF-κB activation induced by overexpression of RANK. In 293 cells stably transfected with full-length RANK, RANKL stimulation facilitates the formation of a complex containing RANK, TRAF6, TAB2, and TAK1, leading to the activation of TAK1. Furthermore, in murine monocyte RAW 264.7 cells, dominant negative forms of TAK1 and TAB2 inhibit NF-κB activation induced by RANKL and endogenous TAK1 is activated in response to RANKL stimulation. These results suggest that the formation of the TRAF6-TAB2-TAK1 complex is involved in the RANK signaling pathway and may regulate the development and function of osteoclasts.

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17

Grimsey, Neil J., Ying Lin, Rachan Narala, Cara C. Rada, Hilda Mejia-Pena, and JoAnn Trejo. "G protein–coupled receptors activate p38 MAPK via a non-canonical TAB1–TAB2– and TAB1–TAB3–dependent pathway in endothelial cells." Journal of Biological Chemistry 294, no. 15 (February 13, 2019): 5867–78. http://dx.doi.org/10.1074/jbc.ra119.007495.

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18

Liu, Delei, Jianghao Liu, Peikan Ye, Haijun Zhang, and Shaowei Zhang. "Low-Temperature, Efficient Synthesis of Highly Crystalline Urchin-like Tantalum Diboride Nanoflowers." Materials 15, no. 8 (April 11, 2022): 2799. http://dx.doi.org/10.3390/ma15082799.

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Urchin-like tantalum diboride (TaB2) nanoflowers were successfully synthesized via a high-efficiency and energy-saving methodology, molten-salt and microwave co-modified boro/carbothermal reduction, using less expensive B4C as a reducing agent. By taking advantage of the synergistic effects of the molten-salt medium and microwave heating conditions, the onset formation temperature of TaB2 was drastically reduced to below 1000 °C, and phase-pure powders of TaB2 nanoflowers were obtained at temperatures as low as 1200 °C within only 20 min. Notably, the present temperature conditions were remarkably milder than those (>1500 °C for several hours) required by conventional reduction methods, which use the strong, but expensive, reducing agent, elemental boron. The resulting urchin-like TaB2 nanoflowers consisted of numerous uniform single-crystalline nanowires with lengths up to 4.16 μm, and high aspect ratios >10. This result indicated that the as-synthesized urchin-like TaB2 nanoflowers possessed high specific surface area and anisotropic morphology, which were favorable not only for sintering, but also for toughening their bulk counterparts.

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19

Takaesu, Giichi, Jun Ninomiya-Tsuji, Satoshi Kishida, Xiaoxia Li, George R. Stark, and Kunihiro Matsumoto. "Interleukin-1 (IL-1) Receptor-Associated Kinase Leads to Activation of TAK1 by Inducing TAB2 Translocation in the IL-1 Signaling Pathway." Molecular and Cellular Biology 21, no. 7 (April 1, 2001): 2475–84. http://dx.doi.org/10.1128/mcb.21.7.2475-2484.2001.

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ABSTRACT Interleukin-1 (IL-1) is a proinflammatory cytokine that recognizes a surface receptor complex and generates multiple cellular responses. IL-1 stimulation activates the mitogen-activated protein kinase kinase kinase TAK1, which in turn mediates activation of c-Jun N-terminal kinase and NF-κB. TAB2 has previously been shown to interact with both TAK1 and TRAF6 and promote their association, thereby triggering subsequent IL-1 signaling events. The serine/threonine kinase IL-1 receptor-associated kinase (IRAK) also plays a role in IL-1 signaling, being recruited to the IL-1 receptor complex early in the signal cascade. In this report, we investigate the role of IRAK in the activation of TAK1. Genetic analysis reveals that IRAK is required for IL-1-induced activation of TAK1. We show that IL-1 stimulation induces the rapid but transient association of IRAK, TRAF6, TAB2, and TAK1. TAB2 is recruited to this complex following translocation from the membrane to the cytosol upon IL-1 stimulation. In IRAK-deficient cells, TAB2 translocation and its association with TRAF6 are abolished. These results suggest that IRAK regulates the redistribution of TAB2 upon IL-1 stimulation and facilitates the formation of a TRAF6-TAB2-TAK1 complex. Formation of this complex is an essential step in the activation of TAK1 in the IL-1 signaling pathway.

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20

Zhou, Qiaoqiao, Cheng Cheng, Yujuan Wei, Jing Yang, Wanzhu Zhou, Qiuyi Song, Mengxiang Ke та ін. "USP15 potentiates NF‐κB activation by differentially stabilizing TAB2 and TAB3". FEBS Journal 287, № 15 (19 січня 2020): 3165–83. http://dx.doi.org/10.1111/febs.15202.

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21

Zhou, Yijia, Yuandong Liao, Chunyu Zhang, Junxiu Liu, Wei Wang, Jiaming Huang, Qiqiao Du, et al. "TAB2 Promotes the Stemness and Biological Functions of Cervical Squamous Cell Carcinoma Cells." Stem Cells International 2021 (June 30, 2021): 1–12. http://dx.doi.org/10.1155/2021/6550388.

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Cancer stem cells are a key population participating in the promotion of the cervical cancer progression through interacting with cancer cells. Existing studies have preliminary revealed that cervical cancer stem cells contribute to tumor recurrence and chemotherapy resistance. However, the specific mechanisms involved in regulating cell functions remain largely unknown. Here, we analyzed published data from public databases and our global transcriptome data, thus identifying cancer-related signaling pathways and molecules. According to our findings, upregulated TAB2 was correlated to stem cell-like properties of cervical cancer. Immunohistochemistry staining of TAB2 in normal and cervical cancer tissues was performed. The cell function experiments demonstrated that knockdown of TAB2 reduced the stemness of cervical cancer cells and, importantly, prevented cervical cancer progression. Collectively, the therapeutic scheme targeting TAB2 may provide an option for overcoming tumor relapse and chemoresistance of cervical cancer via obstructing stemness maintenance.

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22

Matsushita, Junichi, Geum Chan Hwang, and Kwang Bo Shim. "Oxidation Behavior of Tantalum Boride Ceramics." Solid State Phenomena 124-126 (June 2007): 819–22. http://dx.doi.org/10.4028/www.scientific.net/ssp.124-126.819.

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The oxidation behavior of tantalum diboride (TaB2) powder at high temperature was investigated in order to determine the possibility of the use of advanced high temperature structural materials. Unfortunately, monolithic TaB2 were known to be chemical stability up to high temperatures. To date, there have been few reports regarding the properties of TaB2 ceramics. The samples were oxidized at room temperature to 1273 K for 5 minutes to 25 hours in air. The weight changes were measured to estimate the oxidation resistance. The oxidation of samples oxidized for short oxidation time of 5 minutes started at 873 K, and the weight gain increased with increasing oxidation temperature. On the other hand, at the oxidation time of above 1 hour, a maximum weight gain value at 973 to 1073 K was observed. However, even if the oxidation temperature was increased an additional weight change slightly occurred. The weight gain of the sample oxidized at 1273 K for 5 minutes to 25 hours was about 40 to 20 % of the theoretical oxidation mass change. According to the powder X-ray diffraction date, the oxidized TaB2 sample was changed to Ta2O5 at 873 K. Finally, the TaB2 showed a good oxidation resistance at high temperature, because the surface film of tantalum oxide (Ta2O5) formed by oxidation acted as an oxidation resistant layer.

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23

Peng, Fei, Yolande Berta, and Robert F. Speyer. "Effect of SiC, TaB2 and TaSi2 additives on the isothermal oxidation resistance of fully dense zirconium diboride." Journal of Materials Research 24, no. 5 (May 2009): 1855–67. http://dx.doi.org/10.1557/jmr.2009.0216.

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The oxidation resistances of ZrB2 containing SiC, TaB2, and TaSi2 additions of various concentrations were studied using isothermal thermogravimetry at 1200, 1400, and 1500 °C, and specimens were further characterized using x-ray diffraction and electron microscopy. Increasing SiC concentration resulted in thinner glassy surface layers as well as thinner ZrO2-rich underlayers deficient in silica. This silica deficiency was argued to occur by a wicking process of interior-formed borosilicate liquid to the initially-formed borosilicate liquid at the surface. Small (3.32 mol%) concentrations of TaB2 additions were more effective at increasing oxidation resistance than equal additions of TaSi2. The benefit of these additives was related to the formation of a zirconium-tantalum boride solid solution during sintering, which during oxidation, fragmented into fine particles of ZrO2 and TaC. These particles resisted wicking of their liquid/glassy borosilicate encapsulation, which increased overall oxidation resistance. With increasing TaB2 or TaSi2 concentration, oxidation resistance degraded, most egregiously with TaB2 additions. In these cases, zirconia dendrites appeared to grow through the glassy layers, providing conduits for oxygen migration.

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24

Horii, Takaaki, Hiromichi Nagasawa, and Jiro Nakayama. "Functional Analysis of TraA, the Sex Pheromone Receptor Encoded by pPD1, in a Promoter Region Essential for the Mating Response in Enterococcus faecalis." Journal of Bacteriology 184, no. 22 (November 15, 2002): 6343–50. http://dx.doi.org/10.1128/jb.184.22.6343-6350.2002.

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ABSTRACT Conjugative transfer of a bacteriocin plasmid, pPD1, of Enterococcus faecalis is induced in response to a peptide sex pheromone, cPD1, secreted from plasmid-free recipient cells. cPD1 is taken up by a pPD1 donor cell and binds to an intracellular receptor, TraA. Once a recipient cell acquires pPD1, it starts to produce an inhibitor of cPD1, termed iPD1, which functions as a TraA antagonist and blocks self-induction in donor cells. In this study, we discuss how TraA transduces the signal of cPD1 to the mating response. Gel mobility shift assays indicated that TraA is bound to a traA-ipd intergenic region, which is essential for cPD1 response. DNase I footprinting analysis suggested the presence of one strong (tab1) and two weak (tab2 and tab3) TraA-binding sites in the intergenic region. Primer extension analysis implied that the transcriptional initiation sites of traA and ipd were located in the intergenic region. Northern analysis showed that cPD1 upregulated and downregulated transcription of ipd and traA, respectively. The circular permutation assay showed that TraA bent a DNA fragment corresponding to the tab1 region, and its angle was changed in the presence of cPD1 or iPD1. From these data, we propose a model that TraA changes the conformation of the tab1 region in response to cPD1 and upregulates the transcription of ipd, which may lead to expression of genes required for the mating response.

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25

Huang, Xingming, Can Shen, Yan Zhang, Qin Li, Kai Li, Yanyun Wang, Yaping Song, Min Su, Bin Zhou, and Wei Wang. "Associations between TAB2 Gene Polymorphisms and Epithelial Ovarian Cancer in a Chinese Population." Disease Markers 2019 (August 14, 2019): 1–9. http://dx.doi.org/10.1155/2019/8012979.

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Background. Epithelial ovarian cancer (EOC) is highly lethal worldwide. Factors involved in the inflammation and hormone-associated signaling pathway play vital roles in EOC carcinogenesis. The transforming growth factor-β- (TGF-β-) activated kinase 1 (MAP3K7) binding protein 2 (TAB2), mediating convergence of inflammatory and estrogen, may be implicated in EOC. The present study is aimed at exploring the association between the TAB2 gene polymorphisms and EOC. Methods. Three single nucleotide polymorphisms (SNPs) (rs237028, rs521845, and rs652921) of TAB2 were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 221 patients and 252 healthy controls. Associations between SNPs and clinical characteristics were performed either with the χ2 test or with Fisher’s exact test. The Kaplan-Meier method and Cox proportional hazard models were used to detect associations between genotypes and overall survival. Results. The rs237028 polymorphism was significantly associated with an increased risk of EOC with an allelic genetic model (A vs. G; OR=1.45; 95%CI=1.07–1.96; P=0.016), dominant genetic model (AA vs. AG-GG; OR=1.66; CI 1.14–2.41; P=0.008), and overdominant genetic model (AA-GG vs. AG; OR=1.60; CI 1.08–2.36; P=0.017). However, no significant association was observed between rs237028 polymorphism and overall survival. Conclusions. Our study indicated that the rs237028 polymorphism in the TAB2 gene was associated with EOC susceptibility and the TAB2 gene might contribute to the initiation of EOC.

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26

Yang, Guangzhi, Boshen Wang, Dawei Sun, Huimin Wang, Mengyao Chen, Hao Chen, and Baoli Zhu. "Genetic association study between TAB2 polymorphisms and noise-induced-hearing-loss in a Han Chinese population." PLOS ONE 16, no. 5 (May 11, 2021): e0251090. http://dx.doi.org/10.1371/journal.pone.0251090.

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Noise-induced-hearing-loss(NIHL) is a common occupational disease caused by various environmental and biological factors. To investigate the association between TAB2 and the susceptibility of NIHL of people exposed to occupational environments, a genetic association study was performed on selected companies with 588 cases and 537 healthy control subjects. Five selected single nucleotide polymorphisms (SNPs) in TAB2,incoluding rs2744434, rs521845, rs652921, rs7896, rs9485372, were genotyped after a collection of DNA samples. Evident differences in participants between the case group and the control group reveals the result that people with the TAB2 has a high probability of getting NIHL. The results show that rs521845 is deeply associated with the risk of NIHL and is available for the diagnosis in the future.

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27

Ren, Xuanru, Junshuai Lv, Wei Li, Yuwen Hu, Ke Sun, Can Ma, Hong’ao Chu, et al. "Influence of MoSi2 on oxidation protective ability of TaB2-SiC coating in oxygen-containing environments within a broad temperature range." Journal of Advanced Ceramics 9, no. 6 (August 13, 2020): 703–15. http://dx.doi.org/10.1007/s40145-020-0406-5.

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AbstractTaB2-SiC coating modified by different content of MoSi2 was fabricated on graphite substrate with SiC inner coating by liquid phase sintering to elevate the anti-oxidation capability of the TaB2-SiC coatings. As compared to the sample with the TaB2—40wt%SiC coating, the coating sample modified with MoSi2 exhibited a weight gain trend at lower temperatures, the fastest weight loss rate went down by 76%, and the relative oxygen permeability value reduced from about 1% to near 0. More importantly, the large amount of SiO2 glass phase produced over the coating during oxidation was in contact with the modification of MoSi2, which was proved to be beneficial to the dispersion of Ta-oxides. A concomitantly formed continuous Ta-Si-O-B compound glass layer showed excellent capacity to prevent oxygen penetration. However, when the TaB2 content was sacrificed to increase the MoSi2 content, the relative oxygen permeability of the coating increased instead of decreased. Thus, on the basis of ample TaB2 content, increasing the MoSi2 content of the coating is conducive to reducing the relative oxygen permeability of the coatings in a broad temperature region.

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28

Wang, Mingjun, Chen Ling, Jing Cao, Yufeng Yin, Xin Chang, Jian Wu, and Tao Cheng. "Role of Tripartite Motif-Containing 3 Protein (TRIM3) in Rheumatoid Arthritis and Its Mechanism." Journal of Biomaterials and Tissue Engineering 12, no. 9 (September 1, 2022): 1878–84. http://dx.doi.org/10.1166/jbt.2022.3131.

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Aim: To discuss TRIM3’s effects and relative mechanisms in RA development. Materials and methods: Using FLS as research object in our study. Present study divided into two steps, first step, discussing TRIM3 depressing effects in normal FLS cell; next, using IL-1β stimulating to make RA cell model, TRIM3 overexpression in RA model to observe cell biological activities. Measuring IL-6 and TNF-α levels by ELISA kit; evaluating cell proliferation by MTT and EdU assay; relative proteins including TRIM3, TAB2 and NF-κB(p65) proteins expression using WB method. Results: With TRIM3 knockdown, FLS cell proliferation were significantly increased with IL-6, TNF-α levels significantly up-regulation (P < 0.001, respectively). Meanwhile, TAB2 protein expression significantly depressing and NF-κB(p65) protein significantly increasing; those were similar as IL-1β stimulating RA cell model in FLS cell line. In RA cell model, transfection TRIM3 in FLS cell, the cell proliferation was significantly depressed with IL-1β, TNF-α levels depressing, and TAB2 protein expression significantly increasing and NF-κB(p65) protein significantly depressing. Conclusion: TRIM3 knockdown might be a result to RA development; with TRIM3 overexpression, RA induced FLS hyperproliferation significantly improved with TAB2 up-regulation and NF-κB(p65) down-regulation in vitro.

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29

Ishitani, T. "Role of the TAB2-related protein TAB3 in IL-1 and TNF signaling." EMBO Journal 22, no. 23 (December 1, 2003): 6277–88. http://dx.doi.org/10.1093/emboj/cdg605.

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30

Kanayama, Atsuhiro, Rashu B. Seth, Lijun Sun, Chee-Kwee Ea, Mei Hong, Abdullah Shaito, Yu-Hsin Chiu, Li Deng та Zhijian J. Chen. "TAB2 and TAB3 Activate the NF-κB Pathway through Binding to Polyubiquitin Chains". Molecular Cell 15, № 4 (серпень 2004): 535–48. http://dx.doi.org/10.1016/j.molcel.2004.08.008.

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31

Zhang, Yu, Tiantian Gu, Yang Chen, Guoqiang Zhu, Wanwipa Vongsangnak, Qi Xu, and Guohong Chen. "Screening and identification of SipC-interacting proteins in Salmonella enteritidis using Gal4 yeast two-hybrid system in duck." PeerJ 7 (September 13, 2019): e7663. http://dx.doi.org/10.7717/peerj.7663.

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The zoonotic pathogen Salmonella not only reduces the production performance in ducks, but also poses a serious threat to human health through eggs and pollutes water bodies through feces. SipC, an effector protein of type III secretion systems (T3SS) in Salmonella, mediates translocation of effectors into the eukaryotic host. However, the precise role of SipC effectors remains unknown in ducks. In this study, the SipC from duck granulosa cells (dGCs) was selected as bait, and the SipC-interacting proteins in Salmonella enteritidis (SE) were screened using Gal4 yeast two-hybrid system in duck. Twelve SipC-interacting proteins were identified. Among those, the p53-effector related to PMP-22 (PERP) and TGF-β activated kinase 1-binding protein 2 (TAB2) were selected to further confirm the function by GST pull-down in vitro. Over-expression of PERP resulted in not only increasing SE adhesion and invasion but also triggering the production of IL-1β and IFN-α in SE infected dGCs, while knock-down PERP showed the opposite tendency (P < 0.01). In addition, TAB2 significantly induced the production of IL-6, IL-1β, IFN-α, and INF-γ in SE infected dGCs (P < 0.05), but did not cause obvious changes in SE adhesion and invasion. When the sipC in SE was deleted, the activities of duck PERP and TAB2 were abolished because they could not bind to SipC. Taken together, although the protein of PERP and TAB2 can interact with SipC, their mechanisms were different in duck challenged by SE. Therefore, PERP was involved in SE invasion and inflammatory response of dGC ovaries, and TAB2 only contributed to dGCs inflammatory response, which provided critical insights about the mechanism in host- bacterium protein interactions during Salmonella invasion in duck.

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32

Gong, Jian, Xi-Hui Shen, Hui Qiu, Chao Chen та Rong-Ge Yang. "Rhesus monkey TRIM5α represses HIV-1 LTR promoter activity by negatively regulating TAK1/TAB1/TAB2/TAB3-complex-mediated NF-κB activation". Archives of Virology 156, № 11 (15 вересня 2011): 1997–2006. http://dx.doi.org/10.1007/s00705-011-1097-6.

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33

MEHDIKHANI, BEHZAD, GHOLAM HOSSEIN BORHANI, SAEED REZA BAKHSHI, and HAMID REZA BAHARVANDI. "Investigation of TaC–TaB2 ceramic composites." Bulletin of Materials Science 39, no. 1 (February 2016): 79–84. http://dx.doi.org/10.1007/s12034-015-1138-y.

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34

Liu, Qinghang, Jennifer Caldwell Busby, and Jeffery D. Molkentin. "Interaction between TAK1–TAB1–TAB2 and RCAN1–calcineurin defines a signalling nodal control point." Nature Cell Biology 11, no. 2 (January 11, 2009): 154–61. http://dx.doi.org/10.1038/ncb1823.

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35

Zhang, Xiaohong, Gregory E. Hilmas, and William G. Fahrenholtz. "Synthesis, densification, and mechanical properties of TaB2." Materials Letters 62, no. 27 (October 2008): 4251–53. http://dx.doi.org/10.1016/j.matlet.2008.06.052.

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36

Guo, Wei-Ming, Ling-Yong Zeng, Guo-Kang Su, Hao Li, Hua-Tay Lin, and Shang-Hua Wu. "Synthesis of TaB2 powders by borothermal reduction." Journal of the American Ceramic Society 100, no. 6 (April 3, 2017): 2368–72. http://dx.doi.org/10.1111/jace.14824.

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37

Shi, Mude, Weiwen Deng, Enguang Bi, Kairui Mao, Yongyong Ji, Guomei Lin, Xiaodong Wu та ін. "TRIM30α negatively regulates TLR-mediated NF-κB activation by targeting TAB2 and TAB3 for degradation". Nature Immunology 9, № 4 (16 березня 2008): 369–77. http://dx.doi.org/10.1038/ni1577.

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38

Hou, Panpan, Penghui Jia, Kongxiang Yang, Zibo Li, Tian Tian, Yuxin Lin, Weijie Zeng та ін. "An unconventional role of an ASB family protein in NF-κB activation and inflammatory response during microbial infection and colitis". Proceedings of the National Academy of Sciences 118, № 3 (11 січня 2021): e2015416118. http://dx.doi.org/10.1073/pnas.2015416118.

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Nuclear factor κB (NF-κB)–mediated signaling pathway plays a crucial role in the regulation of inflammatory process, innate and adaptive immune responses. The hyperactivation of inflammatory response causes host cell death, tissue damage, and autoinflammatory disorders, such as sepsis and inflammatory bowel disease. However, how these processes are precisely controlled is still poorly understood. In this study, we demonstrated that ankyrin repeat and suppressor of cytokine signaling box containing 1 (ASB1) is involved in the positive regulation of inflammatory responses by enhancing the stability of TAB2 and its downstream signaling pathways, including NF-κB and mitogen-activated protein kinase pathways. Mechanistically, unlike other members of the ASB family that induce ubiquitination-mediated degradation of their target proteins, ASB1 associates with TAB2 to inhibit K48-linked polyubiquitination and thereby promote the stability of TAB2 upon stimulation of cytokines and lipopolysaccharide (LPS), which indicates that ASB1 plays a noncanonical role to further stabilize the target protein rather than induce its degradation. The deficiency of Asb1 protects mice from Salmonella typhimurium– or LPS-induced septic shock and increases the survival of mice. Moreover, Asb1-deficient mice exhibited less severe colitis and intestinal inflammation induced by dextran sodium sulfate. Given the crucial role of ASB proteins in inflammatory signaling pathways, our study offers insights into the immune regulation in pathogen infection and inflammatory disorders with therapeutic implications.

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39

Shim, J. H. "TAK1, but not TAB1 or TAB2, plays an essential role in multiple signaling pathways in vivo." Genes & Development 19, no. 22 (November 15, 2005): 2668–81. http://dx.doi.org/10.1101/gad.1360605.

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40

Braun, Harald, та Jens Staal. "Stabilization of the TAK1 adaptor proteins TAB2 and TAB3 is critical for optimal NF‐κB activation". FEBS Journal 287, № 15 (29 січня 2020): 3161–64. http://dx.doi.org/10.1111/febs.15210.

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41

Shinohara, Hisaaki, Tomoharu Yasuda, and Tomohiro Kurosaki. "TAK1 adaptor proteins, TAB2 and TAB3, link the signalosome to B-cell receptor-induced IKK activation." FEBS Letters 590, no. 18 (August 18, 2016): 3264–69. http://dx.doi.org/10.1002/1873-3468.12342.

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42

Xie, Yanli, Thomas H. Sanders, and Robert F. Speyer. "Solution-Based Synthesis of Submicrometer ZrB2and ZrB2–TaB2." Journal of the American Ceramic Society 91, no. 5 (May 2008): 1469–74. http://dx.doi.org/10.1111/j.1551-2916.2008.02288.x.

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43

Licheri, Roberta, Roberto Orrù, Clara Musa, and Giacomo Cao. "Synthesis, densification and characterization of TaB2–SiC composites." Ceramics International 36, no. 3 (April 2010): 937–41. http://dx.doi.org/10.1016/j.ceramint.2009.10.028.

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44

Ori, Daisuke, Hiroki Kato, Hideki Sanjo, Sarang Tartey, Takashi Mino, Shizuo Akira, and Osamu Takeuchi. "Essential Roles of K63-Linked Polyubiquitin-Binding Proteins TAB2 and TAB3 in B Cell Activation via MAPKs." Journal of Immunology 190, no. 8 (March 15, 2013): 4037–45. http://dx.doi.org/10.4049/jimmunol.1300173.

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45

Zhu, Shu, Wen Pan, Xinyang Song, Yan Liu, Xinrui Shao, Yuanjia Tang, Dong Liang та ін. "The microRNA miR-23b suppresses IL-17-associated autoimmune inflammation by targeting TAB2, TAB3 and IKK-α". Nature Medicine 18, № 7 (3 червня 2012): 1077–86. http://dx.doi.org/10.1038/nm.2815.

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46

Orelio, Claudia, and Elaine Dzierzak. "Identification of 2 novel genes developmentally regulated in the mouse aorta-gonad-mesonephros region." Blood 101, no. 6 (March 15, 2003): 2246–49. http://dx.doi.org/10.1182/blood-2002-07-2260.

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The first adult-repopulating hematopoietic stem cells (HSCs) emerge in the mouse aorta-gonad-mesonephros (AGM) region at embryonic day 10.5 prior to their appearance in the yolk sac and fetal liver. Although several genes are implicated in the regulation of HSCs, there are gaps in our understanding of the processes taking place in the AGM at the time of HSC emergence. To identify genes involved in AGM HSC emergence, we performed differential display reverse transcriptase–polymerase chain reaction (DD RT-PCR). Differentially expressed genes included β-catenin and homologs of human TM9SF2 and TAB2. We characterized the expression pattern of Wnt/β-catenin signaling,mTM9SF2, and mTAB2 in the embryo and adult. Interestingly, the expression of mouse TAB2 (mTAB2) in the E11 dorsal aorta endothelium suggests a role for mTAB2 in HSC emergence and/or regulation. The identification of differentially expressed genes in the AGM region should yield further insights into the development of this tissue and into the emergence and regulation of HSCs.

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47

Rochaix, J. D., K. Perron, D. Dauvillée, F. Laroche, Y. Takahashi, and M. Goldschmidt-Clermont. "Post-transcriptional steps involved in the assembly of photosystem I in Chlamydomonas." Biochemical Society Transactions 32, no. 4 (August 1, 2004): 567–70. http://dx.doi.org/10.1042/bst0320567.

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Assembly of the PSI (photosystem I) complex in eukaryotic photosynthetic organisms depends on the concerted interactions of the nuclear and chloroplast genetic systems. We have identified several nucleus-encoded factors of Chlamydomonas reinhardtii that are specifically required for the synthesis of the two large chloroplast-encoded reaction-centre polypeptides, PsaA and PsaB, of photosystem I and that function at plastid post-transcriptional steps. Raa1, Raa2 and Raa3 are required for the splicing of the three discontinuous psaA precursor transcripts; they are part of large RNA–protein complexes that are reminiscent of spliceosomal particles. Tab1 and Tab2 are involved in the initiation of translation of the psaB mRNA and are localized in the membrane and stromal phases of the chloroplast, where they are associated with high-molecular-mass complexes. Moreover, two chloroplast-encoded proteins, Ycf3 and Ycf4, are required for the primary steps of assembling the photosystem I subunits into a functional complex.

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48

Šroba, Viktor, Tomáš Fiantok, Martin Truchlý, Tomáš Roch, Branislav Grančič, Katarína Viskupová, Leonid Satrapinskyy, et al. "Structure evolution and mechanical properties of Al-alloyed tantalum diboride films prepared by magnetron sputtering co-deposition." Journal of Vacuum Science & Technology A 41, no. 2 (March 2023): 023410. http://dx.doi.org/10.1116/6.0002390.

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Alloying of transition metal diborides with other metals seems to be a suitable way to maintain their excellent mechanical properties under high-temperature loads. Here, we focus on the perspective tantalum diboride (TaB2) hard film, where we investigate the effect of aluminum alloying on the thermally induced structural evolution and mechanical properties of α-Ta1−xAlxB2 using a combination of density functional theory and experiments. Ab initio calculations predict a strong tendency toward the spinodal phase decomposition of the α-TaAlB2 solid solution into isostructural binaries in the entire concentration range at T = 0 K. However, an increase in temperature (T > 773 K) leads to stabilization of the α-Ta1−xAlxB2 solid solution at x < 0.5. The experimental results of magnetron co-sputtered Ta0.75Al0.25B2.14 and Ta0.69Al0.31B2.16 films with aluminum concentrations of 8 and 12.5 at. %, respectively, confirm the insolubility of aluminum in the TaB2 phase. The structure has a nanocomposite character formed by α-TaB2 nanofilaments surrounded by an Al-rich tissue phase. The films are structurally stable up to 1200 °C, but Al atoms already begin to diffuse from the boundary regions when the temperature exceeds 1000 °C. Al alloying causes a decrease in hardness, since the hardness of the reference as-deposited TaB1.21, Ta0.75Al0.25B2.14, and Ta0.69Al0.31B2.16 films is 34, 28, and 27 GPa, respectively. Exposing the films to high temperatures does not lead to a hardening effect; the hardness of Al-depleted films annealed at a temperature of 1200 °C decreased by approximately 10%. The decrease in Young's modulus from 420 GPa (TaB1.21) to 370 GPa (Ta0.69Al0.31B2.16) indicates a tendency toward the ductile behavior of Al alloyed films under mechanical load.

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49

You, Yang, Da-Wang Tan, Wei-Ming Guo, Shang-Hua Wu, Hua-Tay Lin, and Zhuo Luo. "TaB2 powders synthesis by reduction of Ta2O5 with B4C." Ceramics International 43, no. 1 (January 2017): 897–900. http://dx.doi.org/10.1016/j.ceramint.2016.09.193.

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50

Gutierrez, Roberto G., and Peter A. Lachenbruch. "Stata Tip 74: Firstonly, a New Option for Tab2." Stata Journal: Promoting communications on statistics and Stata 9, no. 1 (March 2009): 169–70. http://dx.doi.org/10.1177/1536867x0900900111.

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