Search results for: Twist2




Mammary gland development and EDC-driven cancer susceptibility in mesenchymal ERα-knockout mice.
Development of the mammary gland requires both proper hormone signaling and cross talk between the stroma and epithelium. While estrogen receptor (ERα) expression in the epithelium is essential for normal gland development, the role of this receptor in the stroma is less clear. Moreover, several lines of evidence suggest that mouse phenotypes of in utero exposure to endocrine disruption act through mesenchymal ERα in the developing fetus. We utilized a Twist2-cre mouse line to knock out mesenchymal ERα. Herein, we assessed mammary gland development in the context of mesenchymal ERα deletion. We also tested the effect of in utero bisphenol A (BPA) exposure to alter the tumor susceptibility in the mouse mammary tumor virus-neu (MMTV-neu) breast cancer mouse model. Mesenchymal ERα deletion resulted in altered reproductive tract development and atypical cytology associated with estrous cycling. The mammary gland demonstrated mature epithelial extension unlike complete ERα-knockout mice, but ductal extension was delayed and reduced compared to ERα-competent mice. Using the MMTV-Neu cancer susceptibility model, ERα-intact mice exposed to BPA had reduced tumor-free survival and overall survival compared to BPA-exposed mice having mesenchymal ERα deletion. This difference is specific for BPA exposure as vehicle-treated animals had no difference in tumor development between mice expressing and not expressing mesenchymal ERα. These data demonstrate that mesenchymal ERα expression is not required for ductal extension, nor does it influence cancer risk in this mouse model but does influence the cancer incidence associated with in utero BPA exposure.Clarissa Wormsbaecher, Brittney M Cumbia, Emma G Amurgis, Jillian M Poska, Madeline R Price, Xiaokui M Mo, Sue E Knoblaugh, Takeshi Kurita, Craig Joseph Burd
1887 related Products with: Mammary gland development and EDC-driven cancer susceptibility in mesenchymal ERα-knockout mice.
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Multiple rhabdomyomatous mesenchymal hamartomas in a patient with mosaic Barber-Say syndrome.
Barber-Say syndrome (BSS) is a rare congenital ectodermal dysplasia with few cases reported in the literature. We describe a 9-year-old boy with congenital generalized hypertrichosis and multiple rhabdomyomatous mesenchymal hamartomas (RMHs) on his nose and periocular region. Next-generation sequencing, performed in DNA from a blood sample, and RMH tissue, revealed a pathogenic variant in the TWIST2 gene, which was not detected in a salivary sample of the patient, nor in his parents. Therefore, we consider this variant as de novo mosaicism. To our knowledge, this is the first case of multiple RMHs associated with BSS.Aniza Giacaman, Oriol Corral-Magaña, Carlos Saus Sarrias, Guillermo González-López, Víctor José Asensio Landa, Ana Martín-Santiago
2105 related Products with: Multiple rhabdomyomatous mesenchymal hamartomas in a patient with mosaic Barber-Say syndrome.
16 Arrays/Slide
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Mechanisms of Regulation of the Gene by the TWIST2 and ADD1/SREBP1c Transcription Factors.
Setleis syndrome (SS) is a rare focal facial dermal dysplasia caused by recessive mutations in the basic helix-loop-helix (bHLH) transcription factor, TWIST2. Expression microarray analysis showed that the chordin-like 1 () gene is up-regulated in dermal fibroblasts from three SS patients with the Q119X TWIST2 mutation.José J Casasnovas-Nieves, Yacidzohara Rodríguez, Hector L Franco, Carmen L Cadilla
1092 related Products with: Mechanisms of Regulation of the Gene by the TWIST2 and ADD1/SREBP1c Transcription Factors.
100.00 ul150 IU96500 Units 100 G 100ul100.00 ul
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Retracted: Expression of Dickkopf-1 and Twist2 in Cervical Squamous Cell Carcinoma and Their Correlation with Vasculogenic Mimicry.
[This retracts the article DOI: 10.1155/2022/9288476.].Journal Of Healthcare Engineering
1004 related Products with: Retracted: Expression of Dickkopf-1 and Twist2 in Cervical Squamous Cell Carcinoma and Their Correlation with Vasculogenic Mimicry.
100ug Lyophilized100ug
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Overexpression of SOCS2 Inhibits EMT and M2 Macrophage Polarization in Cervical Cancer via IL-6/JAK2/STAT3 Pathway.
SOCS2 is a member of the suppressor of cytokine signaling (SOCS) protein family associated with the occurrence and development of multiple cancers. This study revealed the expression and molecular mechanisms of SOCS2 in cervical cancer.Dan Li, Yandan Huang, Min Wei, Bin Chen, Yan Lu
1926 related Products with: Overexpression of SOCS2 Inhibits EMT and M2 Macrophage Polarization in Cervical Cancer via IL-6/JAK2/STAT3 Pathway.
2 Pieces/Box
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A stromal lineage maintains crypt structure and villus homeostasis in the intestinal stem cell niche.
The nutrient-absorbing villi of small intestines are renewed and repaired by intestinal stem cells (ISCs), which reside in a well-organized crypt structure. Genetic studies have shown that Wnt molecules secreted by telocytes, Gli1 stromal cells, and epithelial cells are required for ISC proliferation and villus homeostasis. Intestinal stromal cells are heterogeneous and single-cell profiling has divided them into telocytes/subepithelial myofibroblasts, myocytes, pericytes, trophocytes, and Pdgfra stromal cells. Yet, the niche function of these stromal populations remains incompletely understood.Jinnan Xiang, Jigang Guo, Shaoyang Zhang, Hongguang Wu, Ye-Guang Chen, Junping Wang, Baojie Li, Huijuan Liu
1922 related Products with: A stromal lineage maintains crypt structure and villus homeostasis in the intestinal stem cell niche.
96 assays100ug2 Pieces/Box100ug Lyophilized25 ml.100ug Lyophilized100ug Lyophilized
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Promyelocytic leukemia protein regulates angiogenesis and epithelial-mesenchymal transition to limit metastasis in MDA-MB-231 breast cancer cells.
Promyelocytic leukemia protein (PML) modulates diverse cell functions that contribute to both tumor suppressor and pro-oncogenic effects, depending on the cellular context. We show here that PML knockdown (KD) in MDA-MB-231, but not MCF7, breast cancer cells, prolonged stem-cell-like survival, and increased cell proliferation and migration, which is in line with gene-enrichment results from their RNA sequencing analysis. Of note, increased migration was accompanied by higher levels of the epithelial-mesenchymal transition (EMT) regulator Twist-related protein 2 (TWIST2). We showed here that PML binds to TWIST2 via its basic helix-loop-helix (bHLH) region and functionally interferes with the suppression of the epithelial target of TWIST2, CD24. In addition, PML ablation in MDA-MB-231 cells led to higher protein levels of hypoxia-inducible factor 1-alpha (HIF1a), resulting in a higher cell hypoxic response. Functionally, PML directly suppressed the induction of the HIF1a target gene vascular endothelial growth factor A (VEGFa). In line with these results, tumor xenografts of MDA-MB-231 PML-KD cells had enhanced aggressive properties, including higher microvessel density, faster local growth, and higher metastatic ability, with a preference for lung. Collectively, PML suppresses the cancer aggressive behavior by multiple mechanisms that impede both the HIF-hypoxia-angiogenic and EMT pathways.Amalia P Vogiatzoglou, Syrago Spanou, Nikoleta Sachini, Elias Drakos, Christoforos Nikolaou, Takis Makatounakis, Androniki Kretsovali, Joseph Papamatheakis
2457 related Products with: Promyelocytic leukemia protein regulates angiogenesis and epithelial-mesenchymal transition to limit metastasis in MDA-MB-231 breast cancer cells.
100ul
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Genomic insights into the genetic basis of eagle-beak jaw, large head, and long tail in the big-headed turtle.
The big-headed turtle () is an endemic chelonian species in Asia. Unlike most other turtles in the world, is characterized with eagle-beak jaw, large head, and long tail. Although these unique characteristics are well recognized, the underlying genetic basis remains largely elusive. Here, we performed comparative genomic analysis between and other representative species, aiming to reveal the genetic basis of the unique morphological features. Our results revealed that the eagle-beak jaw is most likely enabled by combined effects of expansion of SFRP5, extraction of FGF11, and mutation of both ZFYVE16 and PAX6. Large head is supported by mutations of SETD2 and FGRF2 and copy number variations of six head circumference modulation-related genes (TGFBR2, Twist2, Rdh10, Gas1, Chst11, and SNAP25). The long tail is probably involved in a genetic network comprising Gdf11, Lin 28, and HoxC12, two of which showed a consistent expression pattern with a model organism (mice). These findings suggest that expansion, extraction, and mutation of those genes may have profound effects on unique phenotypes of .Shiping Gong, Yan Ge, Yufeng Wei, Yangchun Gao
1045 related Products with: Genomic insights into the genetic basis of eagle-beak jaw, large head, and long tail in the big-headed turtle.
1100 IU0.1 mg
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Cryptophthalmos: associated syndromes and genetic disorders.
Cryptophthalmos is a rare congenital condition caused by anomalous eyelid development where the eyelid folds do not develop or fail to separate. Cryptophthalmos can be unilateral or bilateral and can occur in isolation or as part of an underlying syndrome. We aim to identify genetic syndromes associated with cryptophthalmos to facilitate genetic diagnosis.Daphna Landau-Prat, Diana H Kim, Sana Bautista, Alanna Strong, Karen E Revere, William R Katowitz, James A Katowitz
1428 related Products with: Cryptophthalmos: associated syndromes and genetic disorders.
500 MG25 mg2.5 mg10 mg100ug100ul50 mg25 mg50 ug 96T100ug10 mg
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