Ask about this productRelated genes to: FBXL14 antibody
- Gene:
- FBXL14 NIH gene
- Name:
- F-box and leucine rich repeat protein 14
- Previous symbol:
- -
- Synonyms:
- MGC40195, Fbl14
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-08
- Date modifiied:
- 2019-02-20
Related products to: FBXL14 antibody
Related articles to: FBXL14 antibody
- : The periosteum and periosteum-derived cells have attracted considerable attention for their potential use in clinical applications for treating bone defects. Bovine periosteum-derived cells have been investigated because of their capability for scaffold-free bone regeneration. Previous mass spectrometry (MS) and immunohistochemistry studies have shown the presence of F-box/leucine-rich repeat protein 14 (FBXL14) in bovine periosteum and periosteum-derived cells. Recently, studies using ESI-Q-Orbitrap MS suggested the presence of type IV collagen in the periosteum. The aim of the present study was to clarify the relationship between type IV collagen and FBXL14 in the formation of periosteum-derived cells. : Bovine periosteum-derived cells were obtained from Japanese Black Cattle's legs in Medium 199 with ascorbic acid and 10% fetal bovine serum. Immunohistochemistry for type IV collagen and FBXL14 was performed using bovine bone with periosteum and periosteum alone for explant culture. : Both type IV collagen and FBXL14 were expressed in Volkmann's canals and the Haversian canals in bone and periosteum. After 5 weeks, type IV collagen and FBXL14 surrounded crystals containing osteocalcin and had formed periosteum-derived cells. Von Kossa staining and immunostaining of osteocalcin revealed that the crystals contained calcified substances and osteocalcin. : Clinically, understanding osteocalcin-interacting proteins will help promote bone regeneration. Interactions between type IV collagen and FBXL14 may contribute to scaffold-free bone regeneration. - Source: PubMed
Publication date: 2025/10/11
Akiyama Mari - β-Hydroxybutyrylation (Kbhb) modification regulates protein molecular fates in either physiology or pathology, including cancer. However, the function and regulatory mechanism of Kbhb remain completely unknown in cancer metastasis. Here, we report that β-hydroxybutyrate (BHB) is clinically associated with the progression of pancreatic cancer and functionally promotes pancreatic cancer cell metastasis. Mechanistically, BHB induces Kbhb modification of Snail at lysine 152 to enhance Snail stabilization, which is regulated by Kbhb modification enzyme CREB-binding protein (CBP), and subsequently prevents Snail degradation by blocking recognition of E3 ubiquitin ligases FBXL14. Furthermore, either targeting Snail Kbhb modification or CBP inhibitor decreases cancer metastasis and enhances the therapeutic efficacy of gemcitabine in pancreatic cancer cells. Collectively, our study reveals that Kbhb of Snail is critical to promote metastasis and provides a potential therapeutic strategy. - Source: PubMed
Publication date: 2025/07/17
Jiang WennaWang MengWang JiayiHao QianhuiLi YuxuanLiu LinZhou TianxingSong WeiLiu JingLiu MiaoXie YongjieZuo DuoXiao JiaweiZhang XiuseGao ShanRen LiHao Jihui - Atherosclerosis is characterized by persistent inflammatory condition, leading to various cardiovascular complications. Foam cell formation, resulting from macrophage uptake of oxidized low-density lipoprotein (ox-LDL), contributes significantly to atherosclerosis progression. This study was designed to investigate the involvement of bispecific phosphatase-6 (DUSP6) and its potential regulatory mechanisms in foam cell formation and atherosclerosis. - Source: PubMed
Publication date: 2025/03/07
Luo WenjieChen YubinFang ChengShi HuiLuo Fanyan - Although the executive pathways of senescence are known, the underlying control mechanisms are diverse and not fully understood, particularly how cancer cells avoid triggering senescence despite experiencing exacerbated stress conditions within the tumor microenvironment. - Source: PubMed
Publication date: 2023/06/20
Gao EnyiSun XiaoyaThorne Rick FrancisZhang Xu DongLi JinmingShao FengminMa JianliWu Mian - Cullin-RING ubiquitin ligases (CRL) regulate numerous biological processes in the heart and have been implicated in regulating cardiac hypertrophy. This study aimed to identify novel hypertrophy-modulating CRLs in cardiomyocytes (CM). A functional genomic approach using siRNA-mediated depletion and automated microscopy was employed to screen for cell size-modulating CRLs in neonatal rat CM. Screening hits were confirmed by H-isoleucine incorporation. Of 43 targets screened, siRNA-mediated depletion of Fbxo6, Fbxo45, and Fbxl14 resulted in decreased cell size, whereas depletion of Fbxo9, Fbxo25, Fbxo30, Fbxo32, Fbxo33, Cullin1, Roc1, Ddb1, Fbxw4, and Fbxw5 led to a markedly increased cell size under basal conditions. In CM stimulated with phenylephrine (PE), depletion of Fbxo6, Fbxo25, Fbxo33, Fbxo45, and Fbxw4 further augmented PE-induced hypertrophy. As a proof-of-concept, the CRL was analysed by transverse aortic constriction (TAC) resulting in a 4.5-fold increase in Fbxo25 protein concentrations compared to control animals. In cell culture, siRNA-mediated depletion of Fbxo25 resulted in a ∼ 37% increase in CM cell size and ∼41% increase in H-isoleucine incorporation. Depleting Fbxo25 resulted in upregulation of Anp and Bnp. In summary, we identified 13 novel CRLs as positive or negative regulators of CM hypertrophy. Of these, CRL was further characterized, as a potential modulator of cardiac hypertrophy. - Source: PubMed
Publication date: 2023/03/08
Fischer MaximillianJakab MoritzHirt Marc NWerner Tessa REngelhardt StefanSarikas Antonio