TBC1D13 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- TBC1D13 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00054662-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- TBC1D13 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: TBC1D13 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- TBC1D13 NIH gene
- Name:
- TBC1 domain family member 13
- Previous symbol:
- -
- Synonyms:
- FLJ10743
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-06
- Date modifiied:
- 2016-10-05
Related products to: TBC1D13 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: TBC1D13 293T Cell Transient Overexpression Lysate(Denatured)
- Endosomal retrieval and recycling of integral cargo proteins is essential for cell and organism development and homeostasis and is orchestrated through a specialised endosomal nanodomain, the retrieval sub-domain. Sub-domain dysfunction is associated with human disease, but our mechanistic understanding of its function remains poorly described. Here, using proximity proteomics of retrieval sub-domain components Retromer and Retriever we identify mechanistic details of retrieval sub-domain composition and organization, including an unrecognised complexity in the interface with RAB GTPase switching. Combining X-ray crystallography and in silico predictions with biochemical and cellular analysis, we reveal that Retromer directly associates and recruits the RAB10 regulators DENND4A, DENND4C, TBC1D1, and TBC1D4, and the RAB35 regulator TBC1D13 to regulate retrieval sub-domain function. The retrieval sub-domain therefore constitutes a hub for integrating cargo recycling with the regulated switching of selected RAB GTPases. We propose this constitutes a major component of the neuroprotective role of the retrieval sub-domain. - Source: PubMed
Publication date: 2025/07/30
Antón-Plágaro CarlosChen Kai-EnGuo QianLiu MeihanEvans Ashley JLewis Philip AHeesom Kate JWilkinson Kevin ACollins Brett MCullen Peter J - Hepatocellular carcinoma (HCC) is a malignancy with a dismal survival rate. The novel autoantibodies panel may provide new insights for the diagnosis of HCC. Biomarkers screened by two methods (bioinformatics and the antigen-antibody system) were taken as candidate tumor-associated antigens (TAAs). Enzyme-linked immunosorbent assay was used to detect the corresponding autoantibodies in 888 samples of verification and validation cohorts. The verification cohort was used to verify the autoantibodies. Samples in the validation cohort were randomly divided into a train set and a test set with the ratio of 6:4. A diagnostic model was established by support vector machines within the train set. The test set further verified the model. Eleven TAAs were selected (AAGAB, C17orf75, CDC37L1, DUSP6, EID3, PDIA2, RGS20, PCNA, TAF7L, TBC1D13, and ZIC2). The titer of six autoantibodies (PCNA, AAGAB, CDC37L1, TAF7L, DUSP6, and ZIC2) had a significant difference in any of the pairwise comparisons among the HCC, liver cirrhosis, and normal control groups. The titer of these autoantibodies had an increasing tendency. Finally, an optimum diagnostic model was constructed with the six autoantibodies. The AUCs were 0.826 in the train set and 0.773 in the test set. The area under the curve (AUC) of this panel for diagnosing early HCC was 0.889. The diagnostic ability of the panel reduced with the progress of HCC. The positive rate of the panel in diagnosing alpha-fetoprotein (AFP)-negative patients was 75.6%. For early HCC, the sensitivity of the combination of AFP with the panel was 90.9% and superior to 53.2% of AFP alone. The novel immunodiagnosis panel combining AFP may be a new approach for the diagnosis of HCC, especially for early-HCC cases. - Source: PubMed
Publication date: 2021/12/14
Wu JinyuWang PengHan ZhuoLi TiandongYi ChunchengQiu CuipengYang QianSun GuiyingDai LipingShi JianxiangWang KeyanYe Hua - The aim of the present study was to investigate key genes in fibroids based on the multiple affinity propogation-Krzanowski and Lai (mAP-KL) method, which included the maxT multiple hypothesis, Krzanowski and Lai (KL) cluster quality index, affinity propagation (AP) clustering algorithm and mutual information network (MIN) constructed by the context likelihood of relatedness (CLR) algorithm. In order to achieve this goal, mAP-KL was initially implemented to investigate exemplars in fibroid, and the maxT function was employed to rank the genes of training and test sets, and the top 200 genes were obtained for further study. In addition, the KL cluster index was applied to determine the quantity of clusters and the AP clustering algorithm was conducted to identify the clusters and their exemplars. Subsequently, the support vector machine (SVM) model was selected to evaluate the classification performance of mAP-KL. Finally, topological properties (degree, closeness, betweenness and transitivity) of exemplars in MIN constructed according to the CLR algorithm were assessed to investigate key genes in fibroid. The SVM model validated that the classification between normal controls and fibroid patients by mAP-KL had a good performance. A total of 9 clusters and exemplars were identified based on mAP-KL, which were comprised of , , , , , , , and . By accessing the topological analysis for exemplars in MIN, and were identified as the two most significant genes of four types of methods, and they were denoted as key genes in the progress of fibroid. In conclusion, two key genes ( and ) and 9 exemplars were successfully investigated, and these may be potential biomarkers for the detection and treatment of fibroid. - Source: PubMed
Publication date: 2017/05/22
Chen Qian-SongWang DanLiu Bao-LianGao Shu-FengGao Dan-LiLi Gui-Rong - Glucose transport is rate limiting for dietary glucose utilization by muscle and fat. The glucose transporter GLUT4 is dynamically sorted and retained intracellularly and redistributes to the plasma membrane (PM) by insulin-regulated vesicular traffic, or 'GLUT4 translocation'. Here we emphasize recent findings in GLUT4 translocation research. The application of total internal reflection fluorescence microscopy (TIRFM) has increased our understanding of insulin-regulated events beneath the PM, such as vesicle tethering and membrane fusion. We describe recent findings on Akt-targeted Rab GTPase-activating proteins (GAPs) (TBC1D1, TBC1D4, TBC1D13) and downstream Rab GTPases (Rab8a, Rab10, Rab13, Rab14, and their effectors) along with the input of Rac1 and actin filaments, molecular motors [myosinVa (MyoVa), myosin1c (Myo1c), myosinIIA (MyoIIA)], and membrane fusion regulators (syntaxin4, munc18c, Doc2b). Collectively these findings reveal novel events in insulin-regulated GLUT4 traffic. - Source: PubMed
Publication date: 2017/06/08
Jaldin-Fincati Javier RPavarotti MartinFrendo-Cumbo ScottBilan Philip JKlip Amira - A putative novel TBC1 domain family member 13 (HqTBC1D13) from Haemaphysalis qinghaiensis was cloned using rapid amplification of the cDNA ends (RACE), the HqTBC1D13 cDNA is 1702bp in length and encodes 396 amino acid residues with predicted molecular weight of 46.09kDa. The TBC-domain containing protein has a catalytic 'arginine finger' analogous to those of Ras and Rho family GAPs, which is critical determinants of GAP activity. The amino acid sequences of TBC domain were evolutionarily highly conserved across species. The partial coding sequence of HqTBC1D13 with the predicted molecular weight of 37.2kDa was expressed and purified in the PGEX-4T-1 vector. Real-time RT PCR analysis showed that the HqTBC1D13 was extensively expressed in the tested organs (salivary glands, midguts, ovaries and cuticles), and its transcriptional levels in salivary glands were significantly up-regulate induced by blood-feeding. The recombinant HqTBC1D13 protein vaccination in the rabbit model resulted in the extension of the duration of feeding and the reduction of 37% female engorgement and 14.8% oviposition compared to the control group. These results indicated that the HqTBC1D13 in ticks could be invovled in the regulation of feeding and oviposition. - Source: PubMed
Publication date: 2016/04/04
Tian ZhanchengDu JunzhengGao ShandianYang JifeiLuo JinXing ShanshanDu XiaoyueLiu GuangyuanLuo JianxunYin Hong