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Memory T cells targeting oncogenic mutations in KRAS, SMAD5, and MUC4 detected in peripheral blood of colon cancer patients have been isolated.
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We demonstrated high expression of miR-145 associated with late stage and unfavorable prognosis of esophageal cancer. We identified SMAD5 as direct target of miR-145, the suppressed expression of which consequently led to increased cell proliferation and migration/invasion.
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Smad5 acts as a intracellular pH messenger and maintains the bioenergetic homeostasis of cells by regulating cytoplasmic metabolic machinery.
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Differential expression of TGF-beta superfamily members and role of Smad1/5/9-signalling in chondral versus endochondral chondrocyte differentiation.
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Data suggest that differences in expression levels in granulosa-like tumor cells and granulosa cells (GCs) from patients with polycystic ovary syndrome (PCOS) are due to increased expression of microRNA-27a-3p in GCs caused by insulin resistance in PCOS; microRNA-27a-3 expression is up-regulated in GCs in PCOS; overexpression of miR-27a-3p inhibits SMAD5 expression and promotes apoptosis. (SMAD5 = SMAD family member 5)
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Here the involvement of the pathway in adult brain function is suggested. This exploratory study establishes a strategy to better identify neuronal molecular signatures that are potentially associated with mental illness and cognitive deficits. We propose that the SMAD pathway may be a novel target in addressing cognitive deficit of SZ in future studies.
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the BMP-2/Smad1/5/RUNX2 signaling pathway participates in the silicon-mediated induction of COL-1 and osteocalcin synth
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miR-23a and miR-27a target SMAD5 and regulate apoptosis in human granulosa cells via the FasL-Fas pathway
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Our findings suggest that suppression of miR-222-3p activity promoted osteogenic differentiation hBMSCs through regulating Smad5-RUNX2 signaling axis.
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Overexpression of the BMP4/SMAD4/SMAD5 signaling pathway could predict poor clinical outcome in skull base chordomas, suggesting activation of this pathway is involved in chordoma pathogenesis.
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The polycomb group protein L3MBTL1 represses a SMAD5-mediated hematopoietic transcriptional program in human pluripotent stem cells.
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adult human Sertoli cells assumed similar morphological features, stable global gene expression profiles and numerous proteins, and activation of AKT and SMAD1/5 during long-period culture.
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balance between Smad1/5- and Smad2/3-dependent signaling defines the outcome of the effect of TGF-beta on atherosclerosis where Smad1/5 is responsible for proatherogenic effects
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among the 15 SNPs, rs3206634 was significantly associated with KD in a recessive model (odds ratio = 2.31, p = 0.019), whereas there was no association between any of the 15 SNPs and CALs.
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Our results indicated that KGN promoted the type-I collagen synthesis of dermal fibroblasts in vitro and in the dermis of mice through activation of the smad4/smad5 pathway.
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Inhibiting Smurf1 mediated ubiquitination of Smad1/5.
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Specific gene siRNAs knock-down further confirmed the osteogenic effects of Genistein on BMP2, SMAD5 and RUNX2 protein expression
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Results indicate that BMP/Smad signaling pathway was altered during the period of osteogenesis, and that the activities of p-Smad1/5 were required for Saos-2 cells viability and differentiation induced by fluoride.
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the shear-induced apoptosis and autophagy are mediated by bone morphogenetic protein receptor type (BMPR)-IB, BMPR-specific Smad1 and Smad5, and p38 mitogen-activated protein kinase.
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a detailed computational model for TGF-beta signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.
