Редактирование: SMAD1

Mothers against decapentaplegic homolog 1 (MAD homolog 1) (Mothers against DPP homolog 1) (JV4-1) (Mad-related protein 1) (SMAD family member 1) (SMAD 1) (Smad1) (hSMAD1) (Transforming growth factor-beta-signaling protein 1) (BSP-1) [BSP1] [MADH1] [MADR1]

==Publications==

{{medline-entry
|title=[[TGFB1]]-Mediated Gliosis in Multiple Sclerosis Spinal Cords Is Favored by the Regionalized Expression of [[HOXA5]] and the Age-Dependent Decline in Androgen Receptor Ligands.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31779094
|abstract=In multiple sclerosis (MS) patients with a progressive form of the disease, spinal cord (SC) functions slowly deteriorate beyond age 40. We previously showed that in the SC of these patients, large areas of incomplete demyelination extend distance away from plaque borders and are characterized by a unique progliotic [[TGFB1]] (Transforming Growth Factor Beta 1) genomic signature. Here, we attempted to determine whether region- and age-specific physiological parameters could promote the progression of SC periplaques in MS patients beyond age 40. An analysis of transcriptomics databases showed that, under physiological conditions, a set of 10 homeobox (HOX) genes are highly significantly overexpressed in the human SC as compared to distinct brain regions. Among these HOX genes, a survey of the human proteome showed that only [[HOXA5]] encodes a protein which interacts with a member of the TGF-beta signaling pathway, namely [[SMAD1]] (SMAD family member 1). Moreover, [[HOXA5]] was previously found to promote the TGF-beta pathway. Interestingly, [[SMAD1]] is also a protein partner of the androgen receptor ([[AR]]) and an unsupervised analysis of gene ontology terms indicates that the [[AR]] pathway antagonizes the TGF-beta/SMAD pathway. Retrieval of promoter analysis data further confirmed that [[AR]] negatively regulates the transcription of several members of the TGF-beta/SMAD pathway. On this basis, we propose that in progressive MS patients, the physiological SC overexpression of [[HOXA5]] combined with the age-dependent decline in [[AR]] ligands may favor the slow progression of [[TGFB1]]-mediated gliosis. Potential therapeutic implications are discussed.
|mesh-terms=* Age Factors
* Aged
* Aging
* Brain
* Data Mining
* Databases, Genetic
* Disease Progression
* Female
* Gene Expression Profiling
* Gliosis
* Homeodomain Proteins
* Humans
* Ligands
* Male
* Middle Aged
* Multiple Sclerosis
* Proteomics
* Receptors, Androgen
* Sequence Analysis, RNA
* Signal Transduction
* Smad1 Protein
* Spinal Cord
* Transforming Growth Factor beta1
* Up-Regulation
|keywords=* androgen receptor
* astrocytes
* homeobox A5
* multiple sclerosis
* spinal cord
* transforming growth factor beta 1
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928867
}}
{{medline-entry
|title=BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27794120
|abstract=Fibrodysplasia ossificans progressiva (FOP) patients carry a missense mutation in [[ACVR1]] [617G > A (R206H)] that leads to hyperactivation of BMP-SMAD signaling. Contrary to a previous study, here we show that FOP fibroblasts showed an increased efficiency of induced pluripotent stem cell (iPSC) generation. This positive effect was attenuated by inhibitors of BMP-SMAD signaling (Dorsomorphin or LDN1931890) or transducing inhibitory SMADs (SMAD6 or SMAD7). In normal fibroblasts, the efficiency of iPSC generation was enhanced by transducing mutant [[ACVR1]] (617G > A) or [[SMAD1]] or adding [[BMP4]] protein at early times during the reprogramming. In contrast, adding [[BMP4]] at later times decreased iPSC generation. ID genes, transcriptional targets of BMP-SMAD signaling, were critical for iPSC generation. The BMP-SMAD-ID signaling axis suppressed p16/INK4A-mediated cell senescence, a major barrier to reprogramming. These results using patient cells carrying the [[ACVR1]] R206H mutation reveal how cellular signaling and gene expression change during the reprogramming processes.
|mesh-terms=* Activin Receptors, Type I
* Adolescent
* Adult
* Animals
* Bone Morphogenetic Proteins
* Cell Line
* Cellular Reprogramming
* Cellular Senescence
* Child
* Cyclin-Dependent Kinase Inhibitor p16
* Female
* Fibroblasts
* Humans
* Induced Pluripotent Stem Cells
* Male
* Mice, Transgenic
* Middle Aged
* Mutation
* Myositis Ossificans
* Signal Transduction
* Smad Proteins
|keywords=* BMP
* FOP
* pluripotency
* reprogramming
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5135304
}}