SMAD1

Last update 08 May 2025

Basic Info

Synonyms

BSP-1, BSP1, hSMAD1

+ [11]

Introduction

Transcriptional modulator that plays a role in various cellular processes, including embryonic development, cell differentiation, and tissue homeostasis (PubMed:9335504). Upon BMP ligand binding to their receptors at the cell surface, is phosphorylated by activated type I BMP receptors (BMPRIs) and associates with SMAD4 to form a heteromeric complex which translocates into the nucleus acting as transcription factor (PubMed:33667543). In turn, the hetero-trimeric complex recognizes cis-regulatory elements containing Smad Binding Elements (SBEs) to modulate the outcome of the signaling network (PubMed:33667543). SMAD1/OAZ1/PSMB4 complex mediates the degradation of the CREBBP/EP300 repressor SNIP1. Positively regulates BMP4-induced expression of odontogenic development regulator MSX1 following IPO7-mediated nuclear import (By similarity).

100 Clinical Results associated with SMAD1

100 Translational Medicine associated with SMAD1

0 Patents (Medical) associated with SMAD1

1,662

Literatures (Medical) associated with SMAD1

01 Apr 2025·International Journal of Biological Macromolecules

Cistanche deserticola polysaccharides enhance female germline stem cell differentiation through BMP/SMAD signaling to mitigate premature ovarian failure

Article

Author: Qiu, Yikai ; Zhang, Yanping ; Li, Xue ; Pei, Xiuying ; Yu, Xiaoli ; Sun, Weiwei ; Li, Jinhua ; Zhang, Qing ; Ouyang, Bangyu ; Wan, Xiuli ; Liu, Xinrui

Female germline stem cells (FGSCs) can self-renew and differentiate into oocytes, replenishing the depleted primordial follicle pool. The traditional Chinese herb, Cistanche deserticola Y.C.Ma, has been used to treat infertility for centuries. Cistanche deserticola polysaccharides (CDPs) are its main active ingredients. In the present study, an animal model of premature ovarian failure (POF) was established to investigate the protective effects of CDPs on the ovary. Ovarian tissue structure and function were assessed after treatment with CDPs, with emphasis on FGSC activation in the ovarian cortex. FGSCs were isolated from newborn mice and treated with CDPs. The morphology, proliferation, expression of stemness, and differentiation markers were evaluated to determine the role of CDPs in promoting FGSC differentiation in vitro. Furthermore, bioinformatics screening identified small mothers against decapentaplegic homologue 9 (Smad9) as a key factor in the signaling pathway. We established a Smad9 differentially expressed cell model using gene modification. We then evaluated changes in the expression of cell stemness maintenance and differentiation ability octamer-binding transcription factor 4 (Oct4), mouse vasa homologue (Mvh), stimulated by retinoic acid gene 8 protein (Stra8), and synaptonemal complex protein 3 (Sycp3) and Smad family markers (SMAD1, SMAD5, SMAD9, SMAD1/5/9, and p-SMAD1/5/9). This approach aimed to verify the molecular mechanism by which CDPs regulate FGSC differentiation through the BMP-SMAD family signaling pathway, ultimately supporting its potential role in improving ovarian function.

01 Apr 2025·Journal of Clinical Investigation

TRIB3 mediates vascular calcification by facilitating self-ubiquitination and dissociation of Smurf1 in chronic kidney disease

Article

Author: Wang, Hao ; Wang, Zhihao ; Zhong, Ming ; Huang, Shanying ; Li, Yihui ; Wang, Feng ; Song, Fangqiang ; Tang, Mengxiong ; Ti, Yun ; Sheng, Yanan ; Guo, Haipeng ; Li, Chen ; Ma, Chang ; Chen, Fangfang ; Sun, Huaibing

The osteogenic environment promotes vascular calcium phosphate deposition and aggregation of unfolded and misfolded proteins, resulting in ER stress in chronic kidney disease (CKD). Controlling ER stress through genetic intervention is a promising approach for treating vascular calcification. In this study, we demonstrated a positive correlation between ER stress-induced tribble homolog 3 (TRIB3) expression and progression of vascular calcification in human and rodent CKD. Increased TRIB3 expression promoted vascular smooth muscle cell (VSMC) calcification by interacting with the C2 domain of the E3 ubiquitin-protein ligase Smurf1, facilitating its K48-related self-ubiquitination at Lys381 and Lys383 and subsequent dissociation from the plasma membrane and nuclei. This degeneration of Smurf1 accelerated the stabilization of the osteogenic transcription factors RUNX family transcription factor 2 (Runx2) and SMAD family member 1 (Smad1). C/EBP homologous protein and activating transcription factor 4 are upstream transcription factors of TRIB3 in an osteogenic environment. Genetic KO of TRIB3 or rescue of Smurf1 ameliorated VSMC and vascular calcification by stabilizing Smurf1 and enhancing the degradation of Runx2 and Smad1. Our findings shed light on the vital role of TRIB3 as a scaffold in ER stress and vascular calcification and offer a potential therapeutic option for CKD.

01 Mar 2025·Biological Psychiatry

A Novel Role for the Histone Demethylase JMJD3 in Mediating Heroin-Induced Relapse-Like Behaviors

Article

Author: Martin, Jennifer A ; Lobo, Mary Kay ; Werner, Craig T ; Higdon, Kate ; Mitra, Swarup ; Neve, Rachel ; Federico, Dale ; An, Chunna ; Dietz, David M ; Shwani, Treefa ; Li, Xiaofang ; Maze, Ian ; Gancarz, Amy M ; Chandra, Ramesh ; Lopez, Ana Garcia ; Gobira, Pedro H ; Thomas, Shruthi A

BACKGROUNDEpigenetic changes that lead to long-term neuroadaptations following opioid exposure are not well understood. We examined how histone demethylase JMJD3 in the nucleus accumbens (NAc) influences heroin seeking after abstinence from self-administration.METHODSMale Sprague Dawley rats were trained to self-administer heroin. Western blotting and quantitative polymerase chain reaction were performed to quantify JMJD3 and bone morphogenetic protein (BMP) pathway expression in the NAc (n = 7-11/group). Pharmacological inhibitors or viral expression vectors were microinfused into the NAc to manipulate JMJD3 or the BMP pathway member SMAD1 (n = 9-11/group). The RiboTag capture method (n = 3-5/group) and viral vectors (n = 7-8/group) were used in male transgenic rats to identify the contributions of D1- and D2-expressing medium spiny neurons in the NAc. Drug seeking was tested by cue-induced response previously paired with drug infusion.RESULTSLevels of JMJD3 and phosphorylated SMAD1/5 in the NAc were increased after 14 days of abstinence from heroin self-administration. Pharmacological and virus-mediated inhibition of JMJD3 or the BMP pathway attenuated cue-induced seeking. Pharmacological inhibition of BMP signaling reduced JMJD3 expression and H3K27me3 levels. JMJD3 bidirectionally affected seeking: expression of the wild-type increased cue-induced seeking whereas expression of a catalytic dead mutant decreased it. JMJD3 expression was increased in D2⁺ but not D1⁺ medium spiny neurons. Expression of the mutant JMJD3 in D2⁺ neurons was sufficient to decrease cue-induced heroin seeking.CONCLUSIONSJMJD3 mediates persistent cellular and behavioral adaptations that underlie heroin relapse, and this activity is regulated by the BMP pathway.

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SMAD1

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