Ask about this productRelated genes to: KREMEN1 antibody
- Gene:
- KREMEN1 NIH gene
- Name:
- kringle containing transmembrane protein 1
- Previous symbol:
- KREMEN
- Synonyms:
- KRM1
- Chromosome:
- 22q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-22
- Date modifiied:
- 2016-04-25
Related products to: KREMEN1 antibody
Related articles to: KREMEN1 antibody
- Among dependence receptors (DRs), which induce apoptosis when unbound by their cognate ligands, Kremen1 was initially reported to drive cancer cell death in the absence of DKK1. However, the precise mechanism of Kremen1-induced cell death remains unclear. In this study, we demonstrate that Kremen1 induces cell death with autophagic features, contrasting with the apoptotic process typically associated with DRs. Functional experiments using pharmacological inhibition of autophagy or genetic silencing of key autophagy effectors, confirmed this cell death process. Protein–protein proximity assays through biotin labeling identified SEC24C, a component of the COP-II complex, as a critical effector of this process. Moreover, the proximity between Kremen1, SEC24C and ATG9A after vesicular trafficking, fosters the proximity of SEC24C with ATG8, ERGIC and ATG9A, likely increasing the number of autophagosomes and vesicles leading to cell death. Given that the Kremen1/DKK1 pair is frequently altered in cancers, its aberrant induction should be monitored and may be targeted to offer an alternative strategy to treat cancers resistant to current therapies. - Source: PubMed
Publication date: 2026/03/11
Brahim SoniaSchott ThomasGhasemi-Firouzabadi ShivaNegulescu AnaGeneste ClaraErrazuriz-Cerda ElisabethIchim GabrielMehlen PatrickMeurette Olivier - Reactive oxygen species (ROS) are critically implicated in ischemic stroke (IS), yet the transcriptional networks and predictive biomarkers underlying ROS dysregulation remain incompletely understood. - Source: PubMed
Publication date: 2026/03/10
Yang LifangLiang TianyuDing Xiaodi - Onychomadesis, characterized by proximal detachment of the nail plate due to temporary arrest of matrix proliferation, has been increasingly recognized as a complication following viral infections. Enterovirus-associated hand-foot-and-mouth disease (HFMD) is the most frequently reported cause. Recent studies demonstrate that some enteroviruses, including Coxsackievirus A10, utilize the host receptor KREMEN1 (KRM1) to impair Wnt/β-catenin signaling and suppress nail stem cell differentiation, thereby providing a molecular basis for infection-induced nail shedding. Additionally, cases of onychomadesis linked to other viral infections, including KRM1-independent enteroviruses, influenza virus, SARS-CoV-2, varicella-zoster virus, and co-infections involving HIV and mpox, have also been documented. Despite growing recognition of the virus-induced onychomadesis, in most cases the exact pathogeneses are yet elusive, thereof lack of approved treatments. Understanding the molecular mechanisms of onychomadesis and other sequelae can enhance diagnostics and therapies, guiding future drug development for virus-induced nail disorders and related complications. A comprehensive literature search was conducted using PubMed up to Dec 2025, including the search terms: onychomadesis, Beau's line, infection or virus, and follow-up. This review aims to explore the molecular pathophysiology of virus-induced onychomadesis and to examine the underlying molecular mechanisms, including the roles of viral receptors and signaling pathways in nail stem cell differentiation. It scrutinizes the currently available literatures of link between viral infections, particularly HFMD, and onychomadesis, focusing on the molecular mechanisms involved, and explores potential therapeutic insights. - Source: PubMed
Publication date: 2026/02/17
Cui YingziSong PuZhao XinTong ZhouGao George Fu - Motor symptoms of Parkinson’s disease (PD) primarily result from the degeneration of nigrostriatal dopaminergic neurons (DANs), particularly the Aldehyde Dehydrogenase 1A1-positive (ALDH1A1⁺) subpopulation. -deficient mice exhibit selective developmental loss of ALDH1A1⁺ DANs but paradoxically display hyperlocomotion, suggesting compensatory changes in striatal circuitry. The dorsal striatum contains four main types of spiny projection neurons (SPNs): patch (or striosome) and matrix subtypes of both direct-pathway (dSPNs) and indirect-pathway (iSPNs). Activation of patch dSPNs suppresses locomotion by inhibiting ALDH1A1⁺ DANs. - Source: PubMed
Publication date: 2026/01/03
Dong JieSullivan Breanna TSmith Victor M MartinezWang LupengTian LuluKung JustinSong BinLin ShirongLe AndreannaSun LixinChang LisaDing JinhuiLe WeidongJia JunCai Huaibin - Motor symptoms of Parkinson's disease (PD) primarily result from the degeneration of nigrostriatal dopaminergic neurons (DANs), particularly the Aldehyde Dehydrogenase 1A1-positive (ALDH1A1) subpopulation. -deficient mice exhibit selective developmental loss of ALDH1A1 DANs but paradoxically display hyperlocomotion, suggesting compensatory changes in striatal circuitry. The dorsal striatum contains four main types of spiny projection neurons (SPNs): patch (or striosome) and matrix subtypes of both direct-pathway (dSPNs) and indirect-pathway (iSPNs). Activation of patch dSPNs suppresses locomotion by inhibiting ALDH1A1 DANs. - Source: PubMed
Publication date: 2025/09/15
Dong JieSullivan Breanna TMartinez Smith Victor MWang LupengTian LuluKung JustinSong BinLin ShirongLe AndreannaSun LixinChang LisaDing JinhuiLe WeidongJia JunCai Huaibin