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 >  Protein>ELAPOR1 >EL1-H82E9

Biotinylated Human ELAPOR1 Protein, His,Avitag™

分子别名(Synonym)

ELAPOR1,Endosome-Lysosome Associated Apoptosis And Autophagy Regulator 1,EIG121,KIAA1324

表达区间及表达系统(Source)

Biotinylated Human ELAPOR1, His,Avitag (EL1-H82E9) is expressed from human 293 cells (HEK293). It contains AA Thr 42 - Lys 910 (Accession # Q6UXG2-1).

Predicted N-terminus: Thr 42

Request for sequence

蛋白结构(Molecular Characterization)

Online(Thr 42 - Lys 910) Q6UXG2-1

This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 99.0 kDa. The protein migrates as 105-125 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

标记(Biotinylation)

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

蛋白标记度(Biotin:Protein Ratio)

Passed as determined by the HABA assay / binding ELISA.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>95% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

Biotinylated Human ELAPOR1, His,Avitag (Cat. No. EL1-H82E9) SDS-PAGE gel

Biotinylated Human ELAPOR1, His,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95%.

 
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背景(Background)

Endosome/lysosome-associated apoptosis and autophagy regulator (ELAPOR1), also known as EIG121 protein, is a type I transmembrane protein induced by estrogen. It is associated with the endosome-lysosome compartments and may play an important role in autophagy and cell proliferation. Under unfavorable conditions such as starvation and exposure to cytotoxic agents, ELAPOR1 may protect cells from cell death by upregulating the autophagy pathway.

 

 

前沿进展

Inceptor binds to and directs insulin towards lysosomal degradation in β cells
Siehler, Bilekova, Chapouton et al
Nat Metab (2024) 6 (12), 2374-2390
Abstract: Blunted first-phase insulin secretion and insulin deficiency are indicators of β cell dysfunction and diabetes manifestation. Therefore, insights into molecular mechanisms that regulate insulin homeostasis might provide entry sites to replenish insulin content and restore β cell function. Here, we identify the insulin inhibitory receptor (inceptor; encoded by the gene IIR/ELAPOR1) as an insulin-binding receptor that regulates insulin stores by lysosomal degradation. Using human induced pluripotent stem cell (SC)-derived islets, we show that IIR knockout (KO) results in enhanced SC β cell differentiation and survival. Strikingly, extended in vitro culture of IIR KO SC β cells leads to greatly increased insulin content and glucose-stimulated insulin secretion (GSIS). We find that inceptor localizes to clathrin-coated vesicles close to the plasma membrane and in the trans-Golgi network as well as in secretory granules, where it acts as a sorting receptor to direct proinsulin and insulin towards lysosomal degradation. Targeting inceptor using a monoclonal antibody increases proinsulin and insulin content and improves SC β cell GSIS. Altogether, our findings reveal the basic mechanisms of β cell insulin turnover and identify inceptor as an insulin degradation receptor.© 2024. The Author(s).
Constructing a Prognostic Model of Uterine Corpus Endometrial Carcinoma and Predicting Drug-Sensitivity Responses Using Programmed Cell Death-Related Pathways
Meng, Zong, Wang et al
J Cancer (2024) 15 (10), 2948-2959
Abstract: Background: Uterine Corpus Endometrial Carcinoma (UCEC) is the most common type of cancer that develops in the uterus, specifically originating from the endometrium, the inner lining of the uterus. Programmed cell death (PCD) is a highly regulated process that eliminates damaged, aged, or unwanted cells in the body. Dysregulation of PCD pathways can contribute to the formation and progression of various cancers, including UCEC. Methods: Fourteen PCD pathways (autophagy-dependent cell death, alkaliptosis, apoptosis, cuproptosis, entotic cell death, ferroptosis, immunogenic cell death, lysosome-dependent cell death, MPT-driven necrosis, necroptosis, netotic cell death, oxeiptosis, parthanatos, and pyroptosis) were involved in building a prognostic signature. The model was trained and tested using data from the TCGA-UCEC and validated with the GSE119041 dataset. Results: A 12-gene PCD signature (DRAM1, ELAPOR1, MAPT, TRIM58, UCHL1, CDKN2A, CYFIP2, AKT2, LINC00618, TTPA, TRIM46, and NOS2) was established and validated in an independent dataset. UCEC patients with a high PCD score (PCDS) exhibited worse prognosis. Furthermore, PCDS was found to be associated with immune related cells and key tumor microenvironment components through multiple methods. It was observed that UCEC patients with a high PCD score may not benefit from immunotherapy, but some chemo drugs like Bortezomib may be useful. Conclusion: In conclusion, a novel PCD model was established by comprehensively analyzing diverse cell death patterns. This model accurately predicts the clinical prognosis and drug sensitivity of UCEC. The findings suggest that the PCD signature can serve as a valuable tool in assessing prognosis and guiding treatment decisions for UCEC patients.© The author(s).
ELAPOR1 induces the classical/progenitor subtype and contributes to reduced disease aggressiveness through metabolic reprogramming in pancreatic cancer
Ohara, Liu, Craig et al
Int J Cancer (2024) 155 (3), 569-581
Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a heterogeneous disease with distinct molecular subtypes described as classical/progenitor and basal-like/squamous PDAC. We hypothesized that integrative transcriptome and metabolome approaches can identify candidate genes whose inactivation contributes to the development of the aggressive basal-like/squamous subtype. Using our integrated approach, we identified endosome-lysosome associated apoptosis and autophagy regulator 1 (ELAPOR1/KIAA1324) as a candidate tumor suppressor in both our NCI-UMD-German cohort and additional validation cohorts. Diminished ELAPOR1 expression was linked to high histological grade, advanced disease stage, the basal-like/squamous subtype, and reduced patient survival in PDAC. In vitro experiments demonstrated that ELAPOR1 transgene expression not only inhibited the migration and invasion of PDAC cells but also induced gene expression characteristics associated with the classical/progenitor subtype. Metabolome analysis of patient tumors and PDAC cells revealed a metabolic program associated with both upregulated ELAPOR1 and the classical/progenitor subtype, encompassing upregulated lipogenesis and downregulated amino acid metabolism. 1-Methylnicotinamide, a known oncometabolite derived from S-adenosylmethionine, was inversely associated with ELAPOR1 expression and promoted migration and invasion of PDAC cells in vitro. Taken together, our data suggest that enhanced ELAPOR1 expression promotes transcriptome and metabolome characteristics that are indicative of the classical/progenitor subtype, whereas its reduction associates with basal-like/squamous tumors with increased disease aggressiveness in PDAC patients. These findings position ELAPOR1 as a promising candidate for diagnostic and therapeutic targeting in PDAC.Published 2024. This article is a U.S. Government work and is in the public domain in the USA. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.
ELAPOR1 suppresses tumor progression in colorectal cancer and indicates favorable prognosis
Huang, Qin, Wu et al
Cancer Biomark (2023) 37 (4), 279-288
Abstract: The role of ELAPOR1 has been evaluated in several cancers but has not been elucidated in colorectal cancer (CRC).To investigate the role of ELAPOR1 in CRC.In the present study, the correlation between ELAPOR1 and survival of CRC patients in TCGA-COAD-READ datasets was predicted, and the difference in ELAPOR1 expression between tumor and normal tissues was analyzed. ELAPOR1 expression in CRC tissues was measured by immunohistochemistry. Then, ELAPOR1 and ELAPOR1-shRNA plasmids were constructed and transfected into SW620 and RKO cells. The effects were assessed by CCK-8, colony formation, transwell, and wound healing assays. Transcriptome sequencing and bioinformatics analysis were performed on the genes before and after ELAPOR1 overexpression in SW620 cells; the differentially expressed genes were substantiated by real-time quantitative reverse transcription PCR.High level of ELAPOR1 is associated with favorable disease-free survival and overall survival. Compared to normal mucosa, ELAPOR1 is lower in CRC. Moreover, ELAPOR1 overexpression significantly inhibits cell proliferation and invasion in vitro in SW260 and RKO cells. Conversely, ELAPOR1-shRNA promotes CRC cell proliferation and invasion. Among the 355 differentially expressed mRNAs identified, 234 were upregulated and 121 were downregulated. Bioinformatics indicated that these genes are involved in receptor binding, plasma membrane, negative regulation of cell proliferation, as well as common cancer signaling pathways.ELAPOR1 plays an inhibitory role in CRC and may be used as a prognostic indicator and a potential target for treatment.
Showing 1-4 of 22 papers.
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