TSC22D4 antibody - N-terminal region (ARP30107_T100)
- Known as:
- TSC22D4 (anti-) - N-terminal region (ARP30107_T100)
- Catalog number:
- arp30107_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TSC22D4 antibody - N-terminal region (ARP30107_T100)
Related genes to: TSC22D4 antibody - N-terminal region (ARP30107_T100)
- Gene:
- TSC22D4 NIH gene
- Name:
- TSC22 domain family member 4
- Previous symbol:
- -
- Synonyms:
- THG-1, TILZ2
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-01
- Date modifiied:
- 2016-10-05
Related products to: TSC22D4 antibody - N-terminal region (ARP30107_T100)
Related articles to: TSC22D4 antibody - N-terminal region (ARP30107_T100)
- To explore the correlation between serum transforming growth factor-β stimulated clone 22 domain family member 4 (TSC22D4) and type 2 diabetes mellitus (T2DM) combined with metabolic associated fatty liver disease (MAFLD). Prospectively, 257 patients with T2DM who were hospitalized at Gansu Provincial Hospital from April 2024 to April 2025 were included in this study, comprising 168 males and 89 females, with the age of [(, )] 53(47, 58) years. Based on their disease status, the patients were divided into the simple T2DM group (=127) and the T2DM+MAFLD group (=130). Additionally, healthy individuals from the physical examination center during the same period were enrolled as the normal control group (=132), including 80 males and 52 females, with the age of 51(47, 57) years. Clinical data were collected, and differences in clinical indicators among the three groups were compared. Spearman correlation analysis was employed to examine the correlations between TSC22D4 and metabolic and inflammatory indicators. A multivariate logistic regression model was employed to analyze the influencing factors of T2DM complicated with MAFLD. The body mass index (BMI), visceral fat area (VFA), fasting blood glucose (FBG), fasting insulin (FINS), homeostasis model assessment of insulin resistance index (HOMA-IR), glycated hemoglobin (HbA1c), TSC22D4, interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) levels were all higher in both the simple T2DM group and the T2DM+MAFLD group compared to the normal control group. Moreover, all these indicators were significantly elevated in the T2DM+MAFLD group compared to the simple T2DM group (all <0.05). Conversely, high-density lipoprotein cholesterol levels were lower in both the simple T2DM group and the T2DM+MAFLD group compared to the normal control group, with the T2DM+MAFLD group exhibiting even lower levels than the simple T2DM group (all <0.05). Among the 257 T2DM patients, Spearman correlation analysis revealed that TSC22D4 was positively correlated with BMI, VFA, FBG, FINS, HOMA-IR, HbA1c, triglycerides, total cholesterol, low-density lipoprotein cholesterol, IL-6, and hs-CRP (all <0.05). The results of the multivariate logistic regression model analysis revealed that elevated BMI (=1.286, 95%:1.128-1.465), longer duration of diabetes (=1.098, 95%:1.036-1.163), and elevated TSC22D4 levels (=1.031, 95%:1.021-1.040) were associated factors contributing to the increased risk of T2DM complicated with MAFLD. Elevated TSC22D4 is a relevant factor contributing to the increased risk of developing T2DM complicated with MAFLD Serum TSC22D4 may contribute to the development and progression of MAFLD in T2DM patients by exacerbating insulin resistance and inflammatory responses. - Source: PubMed
Gao QKang YQuan J XYang ZLi MLiu J X - Transforming growth factor-beta 1 (TGF-β1)-stimulated clone 22 domain (TSC22D) family genes (including ) were identified as transcription factors. It has been demonstrated that they display multiple functions due to proteins' isoforms, redundancy, and other factors. Formerly, researchers mainly focused on its functions, like controlling cell growth and development, cell apoptosis, and balance of osmotic pressure in vivo. Nowadays, growing evidence indicates that they also play an important role in metabolic regulation and the immune system and are expected to be a new potential target for the treatment of diabetes or obesity. Despite this, it has been shown that TSC22D family genes have an inhibitory effect in multiple tumors. In this review, we significantly synthesized advances in metabolism, showing that could control lipid accumulation via modulating adipogenesis and adipose differentiation, while could regulate insulin sensitivity and gluconeogenesis by affecting Akt (serine/threonine kinase, also known as protein kinase B, or PKB) phosphorylation. Moreover, we provide novel insights, including the fact that TSC22D family genes function as a double-edged sword in cancer due to the type of tumor and tumor microenvironment (TME). - Source: PubMed
Publication date: 2026/01/22
Shen WenShen CongJiao YangDeng XiaJia JueYuan Guoyue - WNK family kinases are regulated by osmotic stress and control ion homeostasis by activating SPAK and OXSR1 kinases. Using a proximity labeling approach, we found that osmotic stress promotes the association of WNK1 with the NRBP1 pseudokinase and TSC22D2/4 adaptor proteins, results that are confirmed by immunoprecipitation, mass spectrometry, and immunoblotting studies. NRBP1 pseudokinase is closely related to WNK isoforms and contains a RΦ-motif-binding conserved C-terminal (CCT) domain, like the CCT domains in WNKs, SPAK, and OXSR1. Knockdown or knockout of NRBP1 markedly inhibited basal as well as sorbitol-induced activation of WNK1 and downstream components. We demonstrate that recombinant NRBP1 can directly induce the activation of WNK4 in vitro. AlphaFold-3 modeling predicts that WNK1, SPAK, NRBP1, and TSC22D4 form a complex, in which two TSC22D4 RΦ-motifs interact with the CCTL1 domain of WNK1 and the CCT domain of NRBP1. Our data indicate that NRBP1 and likely its close homolog NRBP2 function as an upstream activator of the WNK pathway. - Source: PubMed
Publication date: 2025/07/16
Amnekar Ramchandra VDite TobyLis PawelBell SebastianBrown FionaJohnson ClareWilkinson StuartRaggett SamanthaDorward MarkWightman MelMacartney ThomasSoares Renata FLamoliatte FredericAlessi Dario R - Insulin resistance (IR) is a critical component of metabolic syndrome, primarily linked to obesity. It contributes to impaired glucose metabolism, beta-cell dysfunction, and the onset of type 2 diabetes. This study aimed to develop a DNAsome nanocarrier designed for the targeted delivery of small interfering RNA (siRNA) to inhibit mRNA of Transforming growth factor beta-like Stimulated Clone 22 D4 (TSC22D4), thereby enhancing insulin sensitivity in hepatocytes. - Source: PubMed
Mohammadi AmenehEbrahimnejad PedramAbediankenari SaidKashi ZahraGill Pooria - Malignant neoplasms arise within a region of chronic inflammation, which is a key factor in all aspects of tumorigenesis including initiation, proliferation, invasion, angiogenesis, and metastasis. IL-1 plays critical functions in tumor development by influencing the tumor microenvironment and promoting cancer progression. However, the mechanism of continuous activation of the IL-1-mediated inflammatory pathway in tumors has not been fully elucidated. This study provides a novel mechanism of the autocrine activation of IL-1 signaling in squamous cell carcinoma (SCC) through a novel oncoprotein, TSC-22 homologous gene-1 (THG-1, also known as TSC22D4). The RNA sequencing analysis revealed that THG-1 overexpression enhances the transcription of NF-κB targets including IL1A, IL1B, TNFA, and IL8. Furthermore, THG-1 knockdown reduced the responsiveness to IL-1 through the suppression of NF-κB nuclear translocation. To elucidate the mechanism, we focused on a THG-1 interacting protein, NRBP1. We found that NRBP1 facilitates the degradation of TNF receptor-associated factor 6 (TRAF6) through its E3 ubiquitin ligase activity. THG-1 bound to NRBP1 and suppressed the degradation of TRAF6. Furthermore, THG-1 knockdown reduced TRAF6 abundance and NF-κB activity in SCC cells. Public database analyses of head and neck SCC revealed that high expression of THG-1 is associated with the activation of the IL-1 and TNF pathways, which share TRAF6 in the signal transductions. Finally, THG-1 abundance in laryngeal SCC specimens is elevated in patients with recurrence. These results indicated that THG-1 drives the self-sufficiency of IL-1-mediated inflammatory pathway, which could contribute to the future diagnosis and immunotherapy of SCCs. Implications: An oncoprotein, THG-1/TSC22D4 activates the IL-1-mediated inflammatory pathway through the suppression of TRAF6 degradation, which mediates the continuous inflammation in tumors. - Source: PubMed
Okano YasuhitoSuzuki HiroyukiWatanabe YukihideAbdelaziz MohammedManevich LevKawanishi KunioOzaki HarukaIshii RyotaMatsumoto ShinGoto NoharaZheng LingOkita YukariHwang JongchanNakayama MasahiroShima YoshihideSakamoto NoriakiNoguchi MasayukiTabuchi KeijiKato Mitsuyasu