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Relevant bibliographies by topics / TGFbeta pathway

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Journal articles

Academic literature on the topic 'TGFbeta pathway'

Author: Grafiati

Published: 1 April 2023

Last updated: 7 July 2024

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Journal articles on the topic "TGFbeta pathway"

1

Verma, Amit. "Presentation name: TGFbeta pathway targeting." Leukemia Research 108 (September 2021): 106682.8. http://dx.doi.org/10.1016/j.leukres.2021.106682.8.

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2

Weiss, Alexander, and Liliana Attisano. "The TGFbeta Superfamily Signaling Pathway." Wiley Interdisciplinary Reviews: Developmental Biology 2, no. 1 (2012): 47–63. http://dx.doi.org/10.1002/wdev.86.

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3

Krishna, S., L. L. Maduzia, and R. W. Padgett. "Specificity of TGFbeta signaling is conferred by distinct type I receptors and their associated SMAD proteins in Caenorhabditis elegans." Development 126, no. 2 (1999): 251–60. http://dx.doi.org/10.1242/dev.126.2.251.

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In C. elegans, the TGFbeta-like type II receptor daf-4 is required for two distinct signaling pathways. In association with the type I receptor daf-1, it functions in the dauer pathway. In addition, it is also required for body size determination and male tail patterning, roles which do not require daf-1. In an effort to determine how two different signals are transmitted through daf-4, we looked for other potential signaling partners for DAF-4. We have cloned and characterized a novel type I receptor and show that it is encoded by sma-6. Mutations in sma-6 generate the reduced body size (Sma)

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4

Tran, Dat Q., Ellen Regalado, and Dianna Milewicz. "Immune Perturbation In Patients With Tgfbeta Pathway Defects." Journal of Allergy and Clinical Immunology 133, no. 2 (2014): AB248. http://dx.doi.org/10.1016/j.jaci.2013.12.881.

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5

Wang, ZacK Z., Hao Bai, Melanie Arzigian, Yong-Xing Gao, and Wen-Shu Wu. "BMP4 and TGFbeta Differentially Regulate CD34+ Progenitor Development in Human Embryonic Stem Cells through SMAD-Dependent Pathway." Blood 112, no. 11 (2008): 889. http://dx.doi.org/10.1182/blood.v112.11.889.889.

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Abstract Pluripotent stem cells derived from patients, including embryonic stem (ES) cells and “induced pluripotent stem” (iPS) cells, are a promising area of regenerative medical research. A major roadblock toward human clinical therapies using ES cells or iPS cells is to define the factors that direct ES cell differentiation into lineage specific cells. We previously established a simple and efficient human embryonic stem cell (hESC) differentiation system to generate CD34+/CD31+ progenitor cells that gave rise to hematopoietic and endothelial cells (Nat Biotech.25:317, 2007). To advance pot

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6

French, Deborah, Francesca Belleudi, Maria Mauro, et al. "Expression of HPV16 E5 down-modulates the TGFbeta signaling pathway." Molecular Cancer 12, no. 1 (2013): 38. http://dx.doi.org/10.1186/1476-4598-12-38.

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7

Tran, Dat, Ellen Regalado, and Dianna Milewicz. "Immune perturbation in patients with TGFbeta pathway defects (LYM7P.729)." Journal of Immunology 192, no. 1_Supplement (2014): 193.17. http://dx.doi.org/10.4049/jimmunol.192.supp.193.17.

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Abstract Intro: Mutations in TGFbR1, TGFbR2 and SMAD3 are associated with familial thoracic aortic aneurysms and aortic dissections (TAAD). These patients offer an opportunity to study their immune development. Methods: PBMC from TAAD (n=9) and controls (CT, n=8) were analyzed by FACS. Th1 (IFNg) and Th17 (IL17A) were determined with intracellular cytokine staining. Foxp3+ Tregs were detected with anti-Foxp3. CD19+ were analyzed for naive (IgD+CD27-), unswitched (IgD+CD27+) and switched memory (IgD-CD27+). Plasmacytoid (CD303+pDC) and myeloid (CD1c+mDC) were defined within lineage-1 negative p

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8

Tervonen, Topi A., Denis Belitškin, Pauliina Munne, et al. "Abstract 834: Serine protease hepsin regulates tumor growth via TGFbeta-EGFR signaling axis." Cancer Research 82, no. 12_Supplement (2022): 834. http://dx.doi.org/10.1158/1538-7445.am2022-834.

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Abstract Hepsin (encoded by HPN gene) is a type II transmembrane serine protease, which is commonly overexpressed in carcinomas of prostate and breast. Hepsin protein is known to be stabilized by Ras-MAPK pathway signaling, and downstream, this protease regulates the degradation of extracellular matrix (ECM) components and activates growth factor pathways, including hepatocyte growth factor (HGF) and transforming growth factor beta (TGF beta) pathway. However, the impact of the hepsin-dependent signaling on cell proliferation and tumor growth is not well-understood. Therefore, we sought to cla

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9

Tang, S. J., P. A. Hoodless, Z. Lu, et al. "The Tlx-2 homeobox gene is a downstream target of BMP signalling and is required for mouse mesoderm development." Development 125, no. 10 (1998): 1877–87. http://dx.doi.org/10.1242/dev.125.10.1877.

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TGFbeta-related factors are critical regulators of vertebrate mesoderm development. However, the signalling cascades required for their function during this developmental process are poorly defined. Tlx-2 is a homeobox gene expressed in the primitive streak of mouse embryos. Exogenous BMP-2 rapidly activates Tlx-2 expression in the epiblast of E6.5 embryos. A Tlx-2 promoter element responds to BMP-2 signals in P19 cells, and this response is mediated by BMP type I receptors and Smad1. These results suggest that Tlx-2 is a downstream target gene for BMP signalling in the primitive streak where

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10

Thatcher, J. D., C. Haun, and P. G. Okkema. "The DAF-3 Smad binds DNA and represses gene expression in the Caenorhabditis elegans pharynx." Development 126, no. 1 (1999): 97–107. http://dx.doi.org/10.1242/dev.126.1.97.

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Gene expression in the pharyngeal muscles of Caenorhabditis elegans is controlled in part by organ-specific signals, which in the myo-2 gene target a short DNA sequence termed the C subelement. To identify genes contributing to these signals, we performed a yeast one-hybrid screen for cDNAs encoding factors that bind the C subelement. One clone recovered was from daf-3, which encodes a Smad most closely related to vertebrate Smad4. We demonstrated that DAF-3 binds C subelement DNA directly and specifically using gel mobility shift and DNase1 protection assays. Mutation of any base in the seque

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