TBC1D4 AS160 antibody Ab host: Goat
- Known as:
- TBC1D4 AS160 (anti-) Antibody production species: Goat
- Catalog number:
- 'AP16672PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- TBC1D4 AS160 antibody host: Goat
Related genes to: TBC1D4 AS160 antibody Ab host: Goat
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
- 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: TBC1D4 AS160 antibody Ab host: Goat
Related articles to: TBC1D4 AS160 antibody Ab host: Goat
- 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 - - Source: PubMed
Publication date: 2026/07/29
Wu NaJing ZuoqianLv HuinaLiu QunGu MingZhong YifanXing PengMa RuiyangJing Yuchen - AS160 (TBC1D4) is a key regulator of glucose transporter trafficking and is frequently overexpressed in several malignancies. However, the mechanisms regulating its protein stability and its contribution to colon tumor metabolism remain poorly understood. Here, we identify a proteotoxic stress-responsive mechanism regulating AS160 abundance that involves crosstalk between the ubiquitin-proteasome system (UPS), ER stress-related signaling, and autophagy. Paradoxically, proteasome inhibition with MG132 resulted in a dose-dependent reduction of AS160 protein levels in both HCT116 and HT29 colon cancer cells, accompanied by the induction of ER stress markers and autophagy activation, including p62 accumulation and increased LC3-II/LC3-I ratios. In contrast, blockade of lysosomal degradation with chloroquine (CHQ) led to marked AS160 accumulation, suggesting that autophagy drives AS160 turnover under proteotoxic stress. Alleviating ER stress with 4-phenylbutyric acid (4-PBA) or scavenging reactive oxygen species with N-acetylcysteine (NAC) did not prevent AS160 loss following MG132 treatment. Functionally, shRNA-mediated knockdown of AS160 did not significantly alter glucose uptake or total GLUT1 protein levels; however, it increased lactate secretion accompanied by reciprocal changes in lactate transporters including upregulation of the lactate transporter MCT4 and downregulation of MCT1. Overall, our results suggest that the stability of AS160 protein is regulated through autophagy-associated pathways and that reduced AS160 expression is associated with altered lactate handling. Targeting pathways that regulate AS160 stability may therefore represent a strategy to modulate tumor metabolic adaptation. - Source: PubMed
Publication date: 2026/04/24
Reabroi SomrudeeSutjarit NareeratChairoungdua Arthit