TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3. Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21WAF1 promoter by binding a T-element close to its initiator. Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21WAF1
TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3. Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21WAF1 promoter by binding a T-element close to its initiator. Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21WAF1
TBS 19, TBX19, FLJ26302, TPIT, dJ747L4.1, T-box protein 19, TBS19, T-box transcription factor TBX19, T-box factor, pituitary, FLJ34543, dj747L4.1, T-box 19 ...
Mutations in the human T-box transcription factor gene TBX3 underlie the autosomal dominant disorder known as ulnar-mammary syndrome (UMS; OMIM 181450) (Bamshad et al., 1997). Human TBX3 was identified during an attempt to positionally clone the gene responsible for another developmental disorder, Holt-Oram syndrome, which had been mapped to chromosome 12q. Although it was later found that Holt-Oram syndrome is caused by mutations in the closely linked human TBX5 gene (Basson et al., 1997; Li et al., 1997), mutations in TBX3 were identified in individuals with ulnar-mammary syndrome, a developmental disorder that was also mapped to this chromosomal region (Bamshad et al., 1995; Bamshad et al., 1997). A number of different mutations in TBX3 have been identified in families with ulnar-mammary syndrome, most of which are predicted to encode truncated proteins or missense mutations resulting in loss of function (Coll et al., 2002) (for a review, see Papaioannou, 2001). UMS is fully penetrant but ...
Consistent with the finding that Fas deficiency might also alter homeostasis of conventional immune cell lineages independently of Eomes, we found that the autoimmune manifestations of ALPS were not affected by the T cell-specific deletion of Eomes (Fig. 2E, 2F). This result was not unexpected because independent lines of evidence have uncoupled DN T cell accumulation from the pathogenic autoantibody production of ALPS (3, 4, 9). Whereas B cell- or DC-specific deficiency of Fas is not sufficient to drive DN T cell expansion, either is sufficient to recapitulate the autoantibody production of ALPS (3, 4). CD4+ T cells, DCs, and B cells are still present and Fas-deficient in lpr/lpr, Eomes F/F, Cd4:Cre+ mice, providing a sufficient cellular network for the elaboration of pathogenic autoantibodies. Taken together, these data suggest that the Eomes-dependent DN T cell population is responsible for the lymphoproliferative phenotype but does not appear to be required for the humoral autoimmunity ...
T-box transcription factor TBX22 is a protein that in humans is encoded by the TBX22 gene. TBX22 is a member of a phylogenetically conserved family of proteins that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. Mutations in this gene have been associated with the inherited X-linked disorder, cleft palate with ankyloglossia (tongue-tie), and it is believed to play a major role in human palatogenesis. It has previously been mapped to the long arm of the X chromosome and it has now been demonstrated that mutations in the gene TBX22 are the cause of this syndrome. TBX22 mutations also result in non-syndromic cleft palate in some populations. TBX22 is composed of seven exons spanning 8.7 kilobases of genomic DNA in Xq21.1. The TBX22 mRNA is 2099 base pairs long and encodes a 400-amino-acids protein containing a T-domain in its NH2-terminal region which has the unique feature of missing 20 amino-acids ...
TY - JOUR. T1 - Expression of the T-box family genes, Tbx1-Tbx5, during early mouse development. AU - Chapman, Deborah L.. AU - Garvey, Nancy. AU - Hancock, Sarah. AU - Alexiou, Maria. AU - Agulnik, Sergei I.. AU - Gibson-Brown, Jeremy J.. AU - Cebra-Thomas, Judith. AU - Bollag, Roni Jacob. AU - Silver, Lee M.. AU - Papaioannou, Virginia E.. PY - 1996/8/1. Y1 - 1996/8/1. N2 - A novel family of genes, characterized by the presence of a region of homology to the DNA-binding domain of the Brachyury (T) locus product, has recently been identified. The region of homology has been named the T-box, and the new mouse genes that contain the T-box domain have been named T-box 1-6 (Tbx1 through Tbx6). As the basis for further study of the function and evolution of these genes, we have examined the expression of 5 of these genes, Tbx1-Tbx5, across a wide range of embryonic stages from blastocyst through gastrulation and early organogenesis by in situ hybridization of wholemounts and tissue sections. Tbx3 is ...
EOMES expression is increased in D*V embryonic comb tissue.Results of qRT-PCR analysis demonstrating increased EOMES expression in D*V embryonic comb tissue whe
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex assemblies. As a member of the wwPDB, the RCSB PDB curates and annotates PDB data according to agreed upon standards. The RCSB PDB also provides a variety of tools and resources. Users can perform simple and advanced searches based on annotations relating to sequence, structure and function. These molecules are visualized, downloaded, and analyzed by users who range from students to specialized scientists.
J:96466 Singh MK, Petry M, Haenig B, Lescher B, Leitges M, Kispert A, The T-box transcription factor Tbx15 is required for skeletal development. Mech Dev. 2005 Feb;122(2):131-44 ...
TY - JOUR. T1 - Specification and determination of limb identity. T2 - Evidence for inhibitory regulation of Tbx gene expression. AU - Saito, Daisuke. AU - Yonei-Tamura, Sayuri. AU - Kano, Kohko. AU - Ide, Hiroyuki. AU - Tamura, Koji. PY - 2002/8/20. Y1 - 2002/8/20. N2 - Limb-type-specific expression of Tbx5/Tbx4 plays a key role in drawing distinction between a forelimb and a hindlimb. Here, we show insights into specification and determination during commitment of limb-type identity, in particular that median tissues regulate Tbx expressions. By using the RT-PCR technique on chick embryos, the onset of specific Tbx5/Tbx4 expression in the wing/leg region was estimated to be stage 13. Specification of the limb-type identity is thought to occur before stage 9, since all explants from stage 9 through 14 expressed the intrinsic Tbx gene autonomously in a simple culture medium. The results of transplantation experiments revealed that axial structures medial to the lateral plate mesoderm at the ...
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TY - JOUR. T1 - TBX3 and its isoform TBX3+2a are functionally distinctive in inhibition of senescence and are overexpressed in a subset of breast cancer cell lines. AU - Fan, Weiwei. AU - Huang, Xu. AU - Chen, Chira. AU - Gray, Joe. AU - Huang, Taosheng. PY - 2004/8/1. Y1 - 2004/8/1. N2 - TBX3 is a transcription factor of the T-box gene family. Mutations of TBX3 cause ulnar-mammary syndrome (MIM 181450) in humans, an autosomal dominant disorder characterized by the absence or underdevelopment of the mammary glands and other congenital anomalies. It recently was found that TBX3 was able to immortalize mouse embryo fibroblast (MEF) cells. In addition, TBX2, a homologue of TBX3, is active in preventing senescence in rodent cells and was found to be amplified in some human breast cancers, suggesting TBX3 plays a role in breast cancer. This study examined the function of TBX3 and its isoform, TBX3 + 2a. TBX3 + 2a differs from TBX3 in the DNA binding domain with an extra 20 amino acids produced by ...
T-box transcription factor 2 Tbx2 is a transcription factor that is encoded by the Tbx2 gene on chromosome 17q21-22 in humans. This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. Tbx2 and Tbx3 are the only T-box transcription factors that act as transcriptional repressors rather than transcriptional activators, and are closely related in terms of development and tumorigenesis. This gene plays a significant role in embryonic and fetal development through control of gene expression, and also has implications in various cancers. Tbx2 is associated with numerous signaling pathways, BMP, TGFβ, Wnt, and FGF, which allow for patterning and proliferation during organogenesis in fetal development. During fetal development, the relationship of Tbx2 to FGF, BMP, and Wnt signaling pathways indicates its extensive control in development of various organ systems. It functions predominantly in the patterning of organ development rather than ...
The T-box transcription factors are a family of developmentally regulated DNA-binding proteins that play important roles in organogenesis (Papaioannou, 2001). Their function is conserved throughout evolution, and they participate in developmental processes such as cell lineage choices, terminal differentiation and proliferation. Notable in both mice and humans is the marked dependency on T-box transcription factor dose, which is evident in the case of dominant human or mouse mutations that lead to several inherited syndromes affecting the heart and other organs (Basson et al., 1997; Bruneau et al., 2001; Li et al., 1997; Lindsay et al., 2001; Merscher et al., 2001; Packham and Brook, 2003; Yagi et al., 2003).. In the heart, T-box genes play important roles in the development of specific cardiac structures and in the transcription of specific cardiac genes. Tbx5 specifies the formation of the posterior segments of the heart, the atria and left ventricle; decreased Tbx5 dose results in defective ...
Buy our Human Tbx20 peptide. Ab99540 is a blocking peptide for ab42468 and has been validated in BL. Abcam provides free protocols, tips and expert support for…
The mouse Brachyury (T) gene is the prototype of a growing family of so-called T-box genes which encode transcriptional regulators and have been identified in a variety of invertebrates and vertebrates, including humans. Mutations in Brachyury and other T-box genes result in drastic embryonic phenotypes, indicating that T-box gene products are essential in tissue specification, morphogenesis and organogenesis. The T-box encodes a DNA-binding domain of about 180 amino-acid residues, the T domain. Here we report the X-ray structure of the T domain from Xenopus laevis in complex with a 24-nucleotide palindromic DNA duplex. We show that the protein is bound as a dimer, interacting with the major and the minor grooves of the DNA. A new type of specific DNA contact is seen, in which a carboxy-terminal helix is deeply embedded into an enlarged minor groove without bending the DNA. Hydrophobic interactions and an unusual main-chain carbonyl contact to a guanine account for sequence-specific recognition ...
The mouse Brachyury (T) gene is the prototype of a growing family of so-called T-box genes which encode transcriptional regulators and have been identified in a variety of invertebrates and vertebrates, including humans. Mutations in Brachyury and other T-box genes result in drastic embryonic phenotypes, indicating that T-box gene products are essential in tissue specification, morphogenesis and organogenesis. The T-box encodes a DNA-binding domain of about 180 amino-acid residues, the T domain. Here we report the X-ray structure of the T domain from Xenopus laevis in complex with a 24-nucleotide palindromic DNA duplex. We show that the protein is bound as a dimer, interacting with the major and the minor grooves of the DNA. A new type of specific DNA contact is seen, in which a carboxy-terminal helix is deeply embedded into an enlarged minor groove without bending the DNA. Hydrophobic interactions and an unusual main-chain carbonyl contact to a guanine account for sequence-specific recognition ...
Abstract B cells contribute to multiple aspects of autoimmune disorders and may play a role in triggering disease. Thus, targeting B cells may be a...
The importance of the BCR and TLR9 in autoimmunity and in the production of autoantibodies is well established but the underlying molecular mechanism still needs to be determined. Here we aim to characterize the BCR-TLR9 crosstalk by its effect on T-bet, as T-bet is activated and regulated by both receptors and has an important role in class-switching to pathological IgG2a in mice. Using primary mouse B cells, we demonstrate that T-bet expression is synergistically elevated by the crosstalk between the BCR and TLR9. To test the effect of this synergy on IgG2a-switching, the levels of switched B cells were checked by functional tests. We found that BCR co-stimulation had no additional effect on TLR9-induced IgG2a expression however the expression of Rad51 was synergistically increased. To check the biological significance of the synergy we compared T-bet expression in B cells from healthy and CIA (collagen-induced arthritis) mice but no differences were found. Taken together, we demonstrate here ...
CD4+ T cells lacking the mTORC1 activator Rheb fail to secrete IFN-γ under Th1 polarizing conditions. We hypothesized that this phenotype is due to defects in regulation of the canonical Th1 transcription factor T-bet at the level of protein phosphorylation downstream of mTORC1. To test this hypothesis, we employed targeted mass-spectrometry proteomic analysis-multiple reaction monitoring mass spectrometry. We used this method to detect and quantify predicted phosphopeptides derived from T-bet. By analyzing activated murine wild-type and Rheb-deficient CD4+ T cells, as well as murine CD4+ T cells activated in the presence of rapamycin, a pharmacologic inhibitor of mTORC1, we were able to identify six T-bet phosphorylation sites. Five of these are novel, and four sites are consistently dephosphorylated in both Rheb-deficient CD4+ T cells and T cells treated with rapamycin, suggesting mTORC1 signaling controls their phosphorylation. Alanine mutagenesis of each of the six phosphorylation sites was ...
Mouse polyclonal antibody raised against a full-length human TBX18 protein. TBX18 (ADR83216.1, 1 a.a. ~ 607 a.a) full-length human protein. (H00009096-B01P) - Products - Abnova
Human TBX3 partial ORF ( NP_005987, 311 a.a. - 410 a.a.) recombinant protein with GST-tag at N-terminal. (H00006926-Q01) - Products - Abnova
EOMES, clone: WD1928, eBioscience™ 25μg; Unconjugated EOMES, clone: WD1928, eBioscience™ Primary Antibodies Eo to Ep
Complete information for TBX3 gene (Protein Coding), T-Box 3, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Given the complexity of Notch receptor and ligand expression during development of the epicardium and the coronary system, we assumed that redundancy between receptors and ligands, respectively, may necessitate the simultaneous removal of 2 or more genes to assign a Notch signaling requirement to these processes. We therefore decided to analyze the phenotypic consequences of removal of Rbpj that encodes a unique intracellular mediator of (canonical) Notch signaling.14 Because Rbpj-deficiency results in early embryonic lethality in mice,15 we used a tissue-specific inactivation approach using a Tbx18cre line generated in our laboratory and a floxed Rbpj allele to analyze Notch signaling function in the PEO and epicardium.10,12 The T-box transcription factor gene Tbx18 is strongly expressed in the PEO at E9.5, and in the epicardium until E16.5. Other cardiac expression domains include the sinus horn mesenchyme/myocardium, and the myocardium of the left ventricle and the interventricular septum ...
Mutation analysis of our cohort of non-deleted patients did not detect any cases with unambiguous loss of TBX1 function. Considering the strong experimental evidence for a major role of TBX1 in the 22q11 deletion syndrome from the deletion studies in the mouse,14-16 our findings are somewhat surprising. In contrast to our results, the majority of mutations inTBX5 in association with Holt-Oram syndrome are predicted to produce haploinsufficiency by nonsense or frameshift mutations within the T box region.12 13 23 Similarly, five of the 10 published mutations in TBX3, found in patients with ulnar-mammary syndrome, are predicted to disrupt the DNA binding domain.24 It is likely that the aetiology of non-deleted DGS/VCFS patients is heterogeneous. Malformations similar to those seen in the 22q11 deletion syndrome have been associated with prenatal exposure to retinoic acids and ethanol, maternal diabetes, and deletions of the short arm of chromosome 10. Therefore, it is possible that mutations ...
In recent years, numerous groups provided compelling evidence for the existence of somatic stem cells in the heart of different mammalian species. Stem cells and progenitor cells are supposed to exist in niches, where they remain in an undifferentiated and quasi-dormant state until external signals stimulate commitment and differentiation to specific somatic cells which may contribute to the repair or maintenance of homeostasis of an organ. Mimicking a stem cell niche of the heart in vitro, we succeeded in the isolation of somatic stem cells from postnatal murine hearts and could maintain these cells as monoclonal self-renewing cells lines expressing Oct4, Sox2 and Nanog for several years (Fig. 1). These cells obviously committed to the mesodermal lineage and expressing early myocardial transcription factors Brachyury, Nkx2.5, GATA4, and Isl1 exclusively differentiate to cardiomyocytes, smooth muscle cells, and vascular endothelial cells and thus were named cardiovascular progenitor cells ...
Abstract. Atrial fibrillation (AF), the most common type of cardiac rhythm disturbance encountered in clinical practice, is associated with substantially increased morbidity and mortality. Aggregating evidence demonstrates that abnormal cardiovascular development is involved in the pathogenesis of AF. A recent study has revealed that the TBX5 gene, which encodes a T-box transcription factor key to cardiovascular development, was associated with AF and atypical Holt-Oram syndrome. However, the prevalence and spectrum of TBX5 mutation in patients with lone AF remain unclear. In this study, the coding regions and splicing junction sites of TBX5 were sequenced in 192 unrelated patients with lone AF and 300 unrelated ethnically-matched healthy individuals used as controls. The causative potential of the identified TBX5 variation was evaluated by MutationTaster and PolyPhen-2. The functional effect of the mutant TBX5 was assayed by using a dual-luciferase reporter assay system. As a result, a novel ...
Several genes containing the conserved T-box region in invertebrates and vertebrates have been reported recently. Here, we describe three novel members of the T-box gene family in zebrafish. One of these genes, tbx-c, is studied in detail. It is expressed in the axial mesoderm, notably, in the notochordal precursor cells immediately before formation of the notochord and in the chordoneural hinge of the tail bud, after the notochord is formed. In addition, its expression is detected in the ventral forebrain, sensory neurons, fin buds and excretory system. The expression pattern of tbx-c differs from that of the other two related genes, tbx-a and tbx-b. The developmental role of tbx-c has been analysed by overexpression of the full-length tbx-c mRNA and a truncated form of tbx-c mRNA, which encodes the dominant-negative Tbx-c. Overexpression of tbx-c causes expansion of the midline mesoderm and formation of ectopic midline structures at the expense of lateral mesodermal cells. In dominant-negative ...
TY - JOUR. T1 - Eomesodermin controls a unique differentiation program in human IL-10 and IFN-γ coproducing regulatory T cells. AU - Gruarin, Paola. AU - Maglie, Stefano. AU - De Simone, Marco. AU - Häringer, Barbara. AU - Vasco, Chiara. AU - Ranzani, Valeria. AU - Bosotti, Roberto. AU - Noddings, Johanna S. AU - Larghi, Paola. AU - Facciotti, Federica. AU - Sarnicola, Maria L. AU - Martinovic, Martina. AU - Crosti, Mariacristina. AU - Moro, Monica. AU - Rossi, Riccardo L. AU - Bernardo, Maria E. AU - Caprioli, Flavio. AU - Locatelli, Franco. AU - Rossetti, Grazisa. AU - Abrignani, Sergio. AU - Pagani, Massimiliano. AU - Geginat, Jens. N1 - © 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.. PY - 2018/11/15. Y1 - 2018/11/15. N2 - Whether human IL-10-producing regulatory T cells ("Tr1") represent a distinct differentiation lineage or an unstable activation stage remains a key unsolved issue. Here, we report that Eomesodermin (Eomes) acted as a lineage-defining transcription factor in human ...
It has been shown that IFN-γ is required for tumor immune surveillance as mice impaired in the secretion of this cytokine are prone to develop spontaneous tumors (25). More recently, it was observed that an IFN-γ-dependent signature and a Th1 immune environment are associated with better prognosis in cancer (10, 12, 13, 23, 26, 27). For instance, good prognosis of ovarian cancer is associated with enhanced Th1 infiltrates and expression of IFN-γ, IL-2, and HLA-class I molecules (27, 28). Similarly, a coordinated cytotoxic Th1 immune phenotype expressing the transcription factor T-box protein 21 (T-bet), interferon regulatory factor 1 (IRF-1), and IFN-γ is associated with good prognosis in colorectal cancer (10, 23). A similar phenomenon was recently reported by our group in breast cancer (13). Interestingly, similar signatures associated with activated IFN-γ signaling are predictive of immune responsiveness to vaccine therapy. Gajewski and colleagues (8, 29) observed that pretreatment ...
TBX5 Full-Length MS Protein Standard (NP_000183), Labeled with [U- 13C6, 15N4]-L-Arginine and [U- 13C6, 15N2]-L-Lysine, was produced in human 293 cells (HEK293) with fully chemically defined cell culture medium to obtain incorporation efficiency at Creative-Proteomics. This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. This gene is closely linked to related family member T-box 3 (ulnar mammary syndrome) on human chromosome 12. The encoded protein may play a role in heart development and specification of limb identity. Mutations in this gene have been associated with Holt-Oram syndrome, a developmental disorder affecting the heart and upper limbs. Several transcript variants encoding different isoforms have been described for this gene.
T-bet is a Type-1 transcription factor that regulates the development of Type-1 T cell and Type-1 anti-tumor immunity. T-bet expression in Dendritic Cells (DC) is required for the ability of these antigen-presenting cells (APC) to prime Type-1-polarized T cell responses. Since T-bet is typically expressed by very low frequencies of activated DC (, 1%), we hypothesized that ectopic expression of T-bet as a consequence of recombinant adenovirus (rAd).T-bet transfection would yield a robust population of DC that were capable of (re)polarizing Type-1 anti-tumor T cell responses in vitro and in vivo. Indeed, human DC engineered to express high levels of T-bet strongly potentiated the development of Type-1 T cells from naïve T cells and concomitantly suppressed Th2 and Regulatory T cell (Treg) development in vitro. Interestingly, the superior Type-1 functionality of DC.Tbet seems to be largely independent of intrinsic Interleukin-12 (IL-12) production, as IL-12 neutralizing antibody failed to affect ...
All organs in the body originate from relatively simple structures in the embryo. For example a simple epithelial tube, the neural tube, develops into the highly complex brain. The many forces and growth factors that act upon embryonic tissues are precisely coordinated to shape the morphogenesis of more complex structures. We are interested in understanding how signalling centres are established in the embryo and how signalling pathways are regulated during development. Current research projects in the lab primarily focus on the fibroblast growth factor (FGF) signalling pathway and our aim is to elucidate how deregulated FGF signalling results in birth defects and cellular malfunction. We are particulalrly interested in understanding the functions of the Sprouty genes, which encode FGF antagonists, Tbx1, a T-box transcription factor implicated in DiGeorge syndrome and Chd7, a chromatin remodeller, mutated in CHARGE syndrome. We are studying the role of these genes in the development of the ...
MSGN1 Full-Length MS Protein Standard (NP_001099039), Labeled with [U- 13C6, 15N4]-L-Arginine and [U- 13C6, 15N2]-L-Lysine, was produced in human 293 cells (HEK293) with fully chemically defined cell culture medium to obtain incorporation efficiency at Creative-Proteomics. Involved in specifying the paraxial, but not dorsal, mesoderm. May regulate the expression of T-box transcription factors required for mesoderm formation and differentiation.
Author summary A molecular understanding of cardiomyocyte development is an essential goal for improving clinical approaches to CHD. While TBX20 is an essential transcription factor for heart development and its disease relevance is well established, many fundamental questions remain about the mechanism of TBX20 function. Principle among these is how TBX20 mutations associated with adult dilated cardiomyopathy circumvent (DCM) the essential embryonic requirement for TBX20 in heart development. Here we report using an integrated approach that TBX20 complexes with the cardiac transcription factor CASZ1 in vivo. We confirmed TBX20 and CASZ1 interact biochemically and genetically, and show mice heterozygous for both Tbx20 and Casz1 die, beginning at 4 to 8 weeks post birth, exhibiting hallmarks of DCM. Interestingly, the human mutant TBX20F256I bypasses the early essential requirement for TBX20 but leads to DCM. We report here that TBX20F256I disrupts the TBX20-CASZ1 interaction, ascribing clinical
B-1 cells and IgM NAbs. In mice, B-1a cells are more properly regarded as an arc of innate immunity. They respond to T cell-independent antigens by secretion of IgM and IgA NAbs, whose repertoire results from natural selection. Importantly, OSEs such as those found on oxLDL and apoptotic cells are a major target of NAbs in both mice and humans (reviewed in ref. 7). Considerable evidence supports an atheroprotective role for IgM specific for OSEs in mice. Immunization of mice with heat-killed S. pneumoniae, which shares molecular identity with oxidized phospholipids of oxLDL, leads to marked increases in IgM specific for oxLDL, which blocks oxLDL uptake by macrophages and inhibits atherosclerosis (79). T-bet deficiency and CD74 deficiency, both associated with reduced atherosclerosis, result in marked increases in IgM NAbs specific for oxLDL (33, 80). Ldlr-/- mice deficient in the ability to secrete IgM (sIgM-/- mice) have dramatically increased atherosclerosis (81). Splenectomy was shown to ...
T-bet Mouse anti-Human, Mouse, PerCP-Cy5.5, Clone: 4B10, eBioscience™ 100μg; PerCP-Cy5.5 T-bet Mouse anti-Human, Mouse, PerCP-Cy5.5, Clone: 4B10,...
This gene is a member of a phylogenetically conserved family of genes that share a common D-binding domain, the T-box. T-box genes encode…
Suppression of cell proliferation by T-bet. Stable T-bet expressing cell clones were established in EcR-HEK cells and maintained in DMEM containing G418 and Zeo
J:63993 Carson CT, Kinzler ER, Parr BA, Tbx12, a novel T-box gene, is expressed during early stages of heart and retinal development. Mech Dev. 2000 Aug;96(1):137-40 ...
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Anti-TBR2 / Eomes antibody - ChIP Grade (ab23345) has been cited in 183 publications. References for Human, Mouse, Rat, Frt, Mmst in ChIP, ChIP/Chip, ICC…
We report here the results of genetic studies on Müllerian aplasia, namely, results of TBX6 and LHX1 mutation screening in 112 MA patients and CNV analysis in a subset of them.. Sequencing of TBX6 (located in 16p11.2) revealed a splice mutation in two patients and rare missense variants in 15 patients (13.4%). TBX6 is a transcription factor that functions in early embryogenesis. It resides on the minus strand with a full-length transcript of 1806 bp, encoding a 436 aminoacid protein (NP_004599.2). TBX6 is a member of a phylogenetically well-conserved T-box gene family, where all members share the similar N-terminal DNA-binding domain, the T-box [55]. We identified a c.622-2A,T splice site mutation in two patients (one with MRKH and the other with total MA and with ovarian aplasia) and a rare homozygous missense variant in exon 4 and exon 6 in two patients. The splice site mutation is situated in the highly conserved splice acceptor site (AG) of exon 5. According to the in silico prediction ...
This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. This protein is a transcriptional repressor and is thought to play a role in the anterior/posterior axis of the tetrapod forelimb. Mutations in this gene cause ulnar-mammary syndrome, affecting limb, apocrine gland, tooth, hair, and genital development. Alternative splicing of this gene results in three transcript variants encoding different isoforms; however, the full length nature of one variant has not been determined ...
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síndrome de Schinzel-Giedion Note Nota The use of the long form of the name, Schinzel-Giedion midface retraction syndrome, is preferred to prevent confusion with Schinzel ulnar-mammary syndrome, a completely unrelated and clinically non-overlapping condition also described by Dr Schinzel. A utilização da forma longa do nome, Schinzel-Giedion Síndrome de retração midface, é o preferido para evitar confusão com Schinzel síndrome ulnar-mamária, completamente independente e clinicamente não-sobreposição condição também descrita pelo Dr. Schinzel. Inheritance Herança Schinzel-Giedion midface retraction syndrome is presumed to be inherited as autosomal recessive on the basis of several pairs of affected sibs with normal parents. Schinzel-Giedion Síndrome de retração midface se presume ser herdada de forma autossômica recessiva, com base em vários pares de irmãos afetados com pais normais. No specific gene or chromosome region has been identified. Nenhum gene específico ou ...
Calcitriol Inhibits the Th1 and Promotes the Th2 Profile in Mice with TNBS Colitis. Th1 lymphocyte differentiation is known to be based on a sequence of cell-intrinsic and exogenous, DC-derived factors, including augmentation of the transcription factor T-bet following activation by DC-derived IL-12. The observed reduction of the Th1 mediators, especially after treatment with the combination of dexamethasone and calcitriol, was further confirmed by immunoblot analysis of the T-bet. The combined administration of calcitriol and dexamethasone led to a significant reduction of T-bet protein expression compared with dexamethasone monotherapy (P , 0.001 versus dexamethasone, Fig. 3, A and B). As a next step to assess a possible role of calcitriol and dexamethasone in promoting the Th2 subset, we analyzed IL-4 production as well as the relevant Th2 lineage commitment factor GATA3. Calcitriol significantly up-regulated IL-4, whereas dexamethasone alone did not cause any significant change in IL-4 ...
The heart is one of the first organs to develop and function in vertebrate embryos. Its formation is a complex process and requires contributions from multiple transcription factors, including GATA-4, eHAND, dHAND, Irx4, and TBX genes [10]. In the developing heart, Tbx5 expression can be first detected at stage 12 along the entire rostrocaudal length of the fused heart tube[11]. Although it is expressed very early in cardiac embryogenesis, Tbx5 is not essential for cardiac crescent formation or for development of the early heart tube. It is at the stage where growth of the posterior segment (atria and left ventricle) of the heart which requires Tbx5, and does not occur in embryos that lack a Tbx5. In contrast, RV and outflow tract development appears to be Tbx5 independent[12]. It is interesting to note that the role of TBX5 in the growth and maturation of posterior heart is evolutionarily conserved from amphibia (Xenopus) to mammals[13]. The signalling mechanism of TBX5 involves interaction ...