Ask about this productRelated genes to: SCUBE3 antibody
- Gene:
- SCUBE3 NIH gene
- Name:
- signal peptide, CUB domain and EGF like domain containing 3
- Previous symbol:
- CEGF3
- Synonyms:
- FLJ34743
- Chromosome:
- 6p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-28
- Date modifiied:
- 2016-01-21
Related products to: SCUBE3 antibody
Related articles to: SCUBE3 antibody
- Dermal papilla (DP) cells orchestrate hair follicle growth and cycling by secreting signaling molecules that stimulate follicular epithelial stem cells. The signal peptide CUB-EGF-like domain-containing protein 3 (SCUBE3) was recently identified as a potent anagen stimulator secreted by DP cells. ethanolic extract (AHE) and its active constituent agerarin exhibit anti-inflammatory properties; however, their effects on hair follicle growth remain unclear. This study aimed to investigate the effects of AHE and agerarin on SCUBE3 expression in primary human DP cells and to elucidate the underlying molecular signaling pathway. Cell viability was assessed by measuring cell confluency. Ex vivo hair growth was analyzed using organ cultures of human hair follicles. Gene and protein expression were determined using reverse transcription-PCR, immunoblot analysis, immunofluorescent staining, tyramide signal amplification-based multiplex immunohistochemistry, and gene promoter-reporter assay in primary human follicle DP cells. In a hair follicle organ culture model, both AHE and agerarin increased the population of the anagen phase and promoted hair shaft elongation. AHE and agerarin significantly upregulated SCUBE3 expression at both the mRNA and protein levels. Mechanistically, AHE and agerarin induced activator protein-1 (AP-1) expression by activating mitogen-activated protein kinase signaling pathways, thereby increasing gene promoter activity. AHE and agerarin promoted hair follicle growth by upregulating SCUBE3 expression via activation of the MAPK-AP-1 signaling axis. In conclusion, AHE and agerarin may serve as potential therapeutic agents for the prevention and treatment of alopecia (hair loss). - Source: PubMed
Publication date: 2026/04/20
Kim YongjinJung EuitaekCho GyungminChoi YenaShin Soon Young - The poor structural stability and insufficient endogenous activation of cartilaginous implant might be key factors for cartilage regeneration after microfracture. Herein, inspired by the restrictive effect of collagen fibers on proteoglycans, we develop artificial proteoglycan assemblies (DSPG@Pep) through sequential co-assembly of bioactive polysaccharide, protein and peptides via electrostatic interactions and covalent conjugation. The DSPG@Pep presents anti-swelling, compression and degradation resistance properties, and significantly activates endogenous stem cell recruitment and direct chondrogenic differentiation. Specifically, the DSPG@Pep downregulates the calcium signaling pathway (e.g., CACNA1G, AVPR1A, et al.) and ECM-receptor interaction (IBSP and COL4A2), thus reduces ossification (EFEMP1, SCUBE3, and SPARCL1) tendency as evidenced by decreased cytosolic calcium concentration and integrin β1 clustering. Cartilage defects models in male rabbits and pigs confirm the DSPG@Pep can be stably immobilized in the defect sites and facilitate the structural and functional remodeling of neocartilage. These findings provide a promising biomaterial design strategy for endogenous cartilage regeneration. - Source: PubMed
Publication date: 2025/12/06
Li ZhulianZhao MingdaZhu JiayiWang YuxiangXiao XiaolinDeng ZhaoxiPeng XuLiu JunliLiang JieJiang QingFan YujiangZhang XingdongSun Yong - Approaches targeting factors that simultaneously promote tumor growth and progression, induce therapy resistance, and inhibit antitumor immunity offer clear benefits over therapies targeting only one of these tumor-promoting processes. Through comprehensive loss-of-function genomic screening, we identified SCUBE3 as a pivotal factor that supports survival and therapy resistance and also orchestrates an immunosuppressive tumor microenvironment. Secretory SCUBE3 supported oncogenic activity through interactions with key oncogenic cell surface receptor proteins, including EGFR, mutant CALR, and TGFβRI/II. These interactions activated the transcription factors FOXR2 and c-Myc, promoting cancer cell proliferation and therapy resistance by enhancing DNA damage repair. Additionally, the SCUBE3-FOXR2 axis created an immunosuppressive tumor microenvironment by facilitating recruitment of the DNMT1 epigenetic repressor complex to the transcription regulator IRF1, thereby inhibiting the expression of MHC-I and MHC-II genes. A first-in-class neutralizing antibody targeting SCUBE3, which was developed using a sophisticated antibody discovery platform and engineered with specific mutations in the heavy chain for enhanced specificity and efficacy, demonstrated profound therapeutic potential across various cancer types in preclinical models, including patient-derived breast and ovarian cancer xenografts. This discovery marks an advancement toward developing a targeted therapy for cancers characterized by hyperactive SCUBE3-associated signaling pathways. - Source: PubMed
Singh DeepikaOnyeagucha Benjamin CMedina DaisySubbarayalu PanneerdossMojidra RahulLv DongwenBhandari MukundTimilsina SantoshPitta Venkata PrabhakarHuang Jian YuNirzhor SaifAbdulsahib ShahadProchnau Jack YancyDo Chris T PRajamanickam SubapriyaChen YidongTaylor Alexander BViswanadhapalli SuryavathiFalzone Maria EJiang JeanSung PatrickZhou DaohongVadlamudi Ratna KHromas RobertRao Manjeet K - The evolutionarily conserved RNA exosome complex modulates gene expression during development. Mutations in RNA exosome complex subunits have been implicated in various human brain disorders, suggesting that defects in RNA decay are linked to impaired neural development. In our study, we identified de novo variants of EXOSC10 in microcephalic individuals. The patient's phenotype can be replicated by heterozygous conditional knockout of Exosc10 in the developing mouse forebrain. The heterozygous loss of Exosc10 in the developing mouse cortex leads to increased cell cycle exit, with a premature differentiation of radial glial cells to intermediate progenitors and neurons in the embryonic cortex. This premature neurogenesis at the expense of neural stem cell proliferation coincides with a smaller cortical size. RNA sequencing and RNA immunoprecipitation sequencing revealed upregulation of many Sonic hedgehog (Shh) signalling genes. We further show the direct degradation of Shh pathway transcripts such as Scube1 and Scube3 by Exosc10. In Exosc10 mouse mutants, the reduced cortical size could be largely rescued by reducing Shh activity. We propose that increased Shh activity due to Exosc10 deficiency leads to premature neurogenesis and ultimately to microcephaly. These observations offer new insights into the neurodevelopmental role of Exosc10 and highlight the dosage-dependent regulation of Shh signalling by Exosc10 in cortical development. - Source: PubMed
Publication date: 2025/10/24
Ulmke Pauline AntonieSakib M SadmanNguyen Dang TonMuchamedin AsisaSokpor GodwinPham LinhXie YuanbinAbbas EmanCastro Hernandez RicardoNarayanan RamanathanWincent JosephineLiedén AgneHarris ElizabethJoss ShelaghFischer AndreStaiger Jochen FNguyen Huu PhucTuoc Tran - Most infants born small for gestational age (SGA) experience catch-up growth within 2 years, while 10% to 15% remain short. The cause of this persistent growth failure remains unknown. - Source: PubMed
Lee YenaJeong Hwal RimKim Eun YoungNoh Eu-SeonJin Hye YoungKwon Eun ByulLee Hye JinPark Sang HeeSeo Young-JunSeo Go HunKim Su JinLee Ji-EunKim Nan YoungHong SangkyoonKang Min JaeHwang Il Tae