AS160 _ TBC1D4 Antibody
- Known as:
- AS160 _ TBC1D4 Antibody
- Catalog number:
- AF1117a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AS160 _ TBC1D4 Antibody
Related genes to: AS160 _ TBC1D4 Antibody
- Gene:
- TBC1D4 NIH gene
- Name:
- TBC1 domain family member 4
- Previous symbol:
- -
- Synonyms:
- KIAA0603, AS160, DKFZp779C0666
- Chromosome:
- 13q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-29
- Date modifiied:
- 2015-11-18
Related products to: AS160 _ TBC1D4 Antibody
Related articles to: AS160 _ TBC1D4 Antibody
- Breast cancer is a major cause of cancer-associated mortality in females. Although therapeutic strategies targeting subtype-specific receptors have been developed for various breast cancer subtypes, effective targeted therapies for triple-negative breast cancer (TNBC) are lacking. Recently, the role of the tumor microenvironment (TME), particularly cancer-associated fibroblasts (CAFs), in the progression and metastasis of breast cancer, especially TNBC, has attracted increasing attention. However, the role of exosomes secreted by CAFs in TNBC cell proliferation is poorly understood. Thus, in this study, we analyzed exosomes derived from both CAFs and MDA-MB-231 cells and identified exosomal miR-1290 as a key component. When delivered to TNBC cells (BT-549 and Hs578T), exosomal miR-1290 directly suppressed the expression of the putative tumor suppressor TBC1D4, which was accompanied by reduced TSC1 expression and activation of the mTOR pathway. The promotion of TNBC cell growth by miR-1290 through direct targeting of TBC1D4 was validated using 2D culture models, 3D spheroid models, and in vivo xenograft models. Furthermore, we demonstrated that treatment with the mTOR inhibitor rapamycin and the FDA-approved rapamycin analog everolimus effectively suppressed miR-1290-induced TNBC cell proliferation, suggesting a potential therapeutic strategy for TNBC. Moreover, in patient cohorts, elevated levels of circulating miR-1290 significantly distinguished patients with breast cancer from healthy individuals and correlated with poor survival outcomes. Therefore, miR-1290 and its direct target TBC1D4 have potential value in both targeted treatment and diagnosis of TNBC. - Source: PubMed
Publication date: 2026/09/20
Lee JinkwonSon TaesangKim GyeonghwaLee Hye WonTae In HwanKang YunsangLee JeongminKim JinsanLee Su-GiHan Tae-HeeBan Hyun SeungPark KunhyangJung Cho-RokLim Jung HwaSon Mi-YoungKim Dae-SooHur KeunHan Tae-SuCho Hyun-Soo - This manuscript is the corrected version of a previously published paper. Glucose uptake by mammalian cells is a key mechanism to maintain cell and tissue homeostasis and relies mostly on plasma membrane-localized glucose transporter proteins (GLUTs). Two main cellular mechanisms regulate GLUT proteins in the cell: first, expression of GLUT genes is under dynamic transcriptional control and is used by cancer cells to increase glucose availability. Second, GLUT proteins are regulated by membrane traffic from storage vesicles to the plasma membrane (PM). This latter process is triggered by signaling mechanisms and is well studied in the case of insulin-responsive cells, which activate protein kinase AKT to phosphorylate TBC1D4, a RAB-GTPase-activating protein involved in membrane traffic regulation. Previously, we identified protein kinase WNK1 as another kinase able to phosphorylate TBC1D4 and regulate the surface abundance of the constitutive glucose transporter GLUT1. Here we describe that downregulation of WNK1 through RNA interference in HEK293 cells led to a two-fold decrease in cell-surface GLUT1 abundance, concomitant with a 40% decrease in glucose uptake. By mass spectrometry, we identified serine (S) 704 in TBC1D4 and also S565 in its paralogue TBC1D1 as candidate WNK1 phosphorylation sites. Transfection of the respective phosphomimetic or unphosphorylatable TBC1D mutants into cells revealed that both affected the cell-surface abundance of GLUT1. The results reinforce a regulatory role for WNK1 in GLUT1 trafficking and glucose uptake and may have potential impact for the understanding of metabolic dysregulation, as observed in many cancer cells or insulin-responsive cell types. - Source: PubMed
Publication date: 2026/08/31
Henriques Andreia F AMatos PauloCarvalho Ana SofiaAzkargorta MikelElortza FelixMatthiesen RuneJordan Peter - Nx3 (novex-3) is an exceptionally small isoform of the giant protein titin, whose structural and functional roles within the sarcomere remain poorly understood. - Source: PubMed
Publication date: 2026/09/10
Linke Wolfgang AKümper LisaFomin AndreyMartin IsabelIgnatyeva NadezdaHashimoto KenMohr ClemensBässler JosefineGärtner AnnaOhira MomokoHanashima AkiraKlotz AnnikaSchiffer KaiVoelkel TobiasFreundt Johanna KHucke AnnaKoser FranziskaZhang TaoHobbach Anastasia JGlass Ian A Gummert Jan FDos Remedios Cristobal Gvan Heesch SebastiaanRuiz-Orera JorgeMohri SatoshiHubner NorbertRegnier MichaelMilting HendrikMayans OlgaUnger AndreasEbert Antje - Regulation of skeletal muscle glucose uptake is an effective strategy for reducing postprandial hyperglycemia and improving whole-body glucose homeostasis in the management of type 2 diabetes. The present study investigated that cardamom enhances glucose uptake in skeletal muscle in vitro and improves glucose tolerance in vivo. Bioactivity-guided fractionation of cardamom identified an ethyl acetate fraction (Fr. A) and its subfraction (Fr. A-i) as potent stimulators of glucose uptake in L6 myotubes. Both fractions significantly promoted glucose uptake by enhancing glucose transporter type 4 (GLUT4) translocation to the plasma membrane. Mechanistic investigations revealed activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, accompanied by increased phosphorylation of Akt substrate of 160 kDa (AS160), a key regulator of GLUT4 vesicle trafficking, while no significant changes were observed in insulin receptor substrate-1 (IRS-1) or AMP-activated protein kinase (AMPK) phosphorylation. Fr. A induced a more pronounced effect on AS160 phosphorylation and was therefore selected for further evaluation. The antihyperglycemic potential of Fr. A was assessed in ICR mice using an oral glucose tolerance test. Oral administration of Fr. A (1 and 10 mg/kg body weight) significantly improved glucose tolerance and alleviated postprandial hyperglycemia. Cardamom in skeletal muscle and highlights its potential as a natural therapeutic candidate for the management of postprandial hyperglycemia. - Source: PubMed
Fang LiyuanHironao Ken-YuAshida HitoshiYamashita Yoko - Monogenic diabetes caused by TBC1D4 mutations is a relatively rare hereditary disorder of glucose metabolism that has increasingly gained attention in recent years. The protein encoded by this gene plays a pivotal regulatory role in glucose transport within skeletal muscle and adipose tissue; its dysfunction leads to significant insulin resistance and glucose dysregulation characterized by predominant postprandial hyperglycemia. Accumulating research indicates that TBC1D4 mutations may contribute to metabolic disturbances by impairing glucose transport and blunting cellular insulin sensitivity. Patients typically present in adolescence or young adulthood, often accompanied by metabolic comorbidities such as obesity, dyslipidemia, fatty liver, and hyperuricemia; some may also manifest acanthosis nigricans or polyendocrine metabolic ovarian syndrome (PMOS; formerly polycystic ovary syndrome)-like features. Due to frequent clinical misdiagnosis or underdiagnosis, a comprehensive evaluation incorporating age of onset, family history, glycemic characteristics, autoantibody status, and genetic testing is essential for accurate diagnosis. Currently, specific targeted therapies are lacking, and lifestyle intervention remains the cornerstone of management, with exercise intervention being particularly vital for improving insulin resistance. This review focuses on the molecular biological characteristics of the TBC1D4 gene and its encoded protein, mutation types, pathogenic mechanisms, clinical manifestations, and diagnostic strategies, as well as therapeutic advances. It aims to systematically summarize the research progress on TBC1D4-related monogenic diabetes to enhance clinical awareness and provide a reference for early identification, precise diagnosis, and individualized treatment. - Source: PubMed
Wang WenjingMa LidanDong BingziGao PeihanSun Xiaofang