Mouse Anti-ERN1 Recombinant Antibody (CB193) (V2LY-0825-LY734)

Name: Mouse Anti-ERN1 Recombinant Antibody (CB193)
SKU: V2LY-0825-LY734
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CB193

Application

ELISA, IHC-P

Immunogen

Recombinant Human ERN1 / IRE1 protein.

Host Species

Mouse

Specificity

Human

Antibody Isotype

IgG2b

Clonality

Monoclonal Antibody

Application Notes

Application	Note
ELISA	1:1000-1:2,000
IHC-P	1:100-1:500

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS

Preservative

None

Concentration

Batch dependent

Purity

> 95% Purity determined by SDS-PAGE.

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

More Infomation

Target

Full Name

Endoplasmic Reticulum To Nucleus Signaling 1

Entrez Gene ID

2081

UniProt ID

O75460

Research Area

Serine/threonine-protein kinase and endoribonuclease that acts as a key sensor for the endoplasmic reticulum unfolded protein response (UPR) (PubMed:11779464, PubMed:11175748, PubMed:12637535, PubMed:9637683, PubMed:21317875, PubMed:28128204).

In unstressed cells, the endoplasmic reticulum luminal domain is maintained in its inactive monomeric state by binding to the endoplasmic reticulum chaperone HSPA5/BiP (PubMed:21317875).

Accumulation of misfolded proteins in the endoplasmic reticulum causes release of HSPA5/BiP, allowing the luminal domain to homodimerize, promoting autophosphorylation of the kinase domain and subsequent activation of the endoribonuclease activity (PubMed:21317875).

The endoribonuclease activity is specific for XBP1 mRNA and excises 26 nucleotides from XBP1 mRNA (PubMed:11779464, PubMed:24508390, PubMed:21317875).

The resulting spliced transcript of XBP1 encodes a transcriptional activator protein that up-regulates expression of UPR target genes (PubMed:11779464, PubMed:24508390, PubMed:21317875).

Acts as an upstream signal for ER stress-induced GORASP2-mediated unconventional (ER/Golgi-independent) trafficking of CFTR to cell membrane by modulating the expression and localization of SEC16A (PubMed:21884936, PubMed:28067262).

Biological Process

Cellular response to glucose stimulus Source: ParkinsonsUK-UCL
Cellular response to hydrogen peroxide Source: Ensembl
Cellular response to unfolded protein Source: ParkinsonsUK-UCL
Cellular response to vascular endothelial growth factor stimulus Source: UniProtKB
Endothelial cell proliferation Source: UniProtKB
Insulin metabolic process Source: ParkinsonsUK-UCL
Intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress Source: GO_Central
IRE1-mediated unfolded protein response Source: UniProtKB
mRNA catabolic process Source: ParkinsonsUK-UCL
mRNA cleavage Source: UniProtKB
mRNA cleavage involved in mRNA processing Source: ParkinsonsUK-UCL
mRNA splicing, via endonucleolytic cleavage and ligation Source: UniProtKB
Peptidyl-serine autophosphorylation Source: ParkinsonsUK-UCL
Peptidyl-serine trans-autophosphorylation Source: ParkinsonsUK-UCL
Positive regulation of endoplasmic reticulum unfolded protein response Source: UniProtKB
Positive regulation of JUN kinase activity Source: ParkinsonsUK-UCL
Positive regulation of RNA splicing Source: UniProtKB
Positive regulation of vascular associated smooth muscle cell proliferation Source: BHF-UCL
Protein autophosphorylation Source: ParkinsonsUK-UCL
Protein phosphorylation Source: UniProtKB
Regulation of cell cycle Source: UniProtKB
Regulation of macroautophagy Source: ParkinsonsUK-UCL
Response to endoplasmic reticulum stress Source: ParkinsonsUK-UCL

Cellular Location

Endoplasmic reticulum membrane

Topology

Lumenal: 19-443
Helical: 444-464
Cytoplasmic: 465-977

PTM

Autophosphorylated following homodimerization. Autophosphorylation promotes activation of the endoribonuclease domain.
ADP-ribosylated by PARP16 upon ER stress, which increases both kinase and endonuclease activities.

Pandeya, A., Khalko, R. K., Singh, S., Kumar, M., & Gosipatala, S. B. (2022). Hcmv-miR-UL148D regulates the staurosporine-induced apoptosis by targeting the Endoplasmic Reticulum to Nucleus signaling 1 (ERN1). Plos one, 17(9), e0275072.

Baeken, M. W., & Yokobayashi, Y. (2022). Identification of an ERN1 target site within EGFP mRNA. Journal of Cellular Biochemistry, 123(8), 1298-1305.

Minchenko, D. O., Khita, O. O., Tsymbal, D. O., Danilovskyi, S. V., Rudnytska, O. V., Halkin, V., ... & Minchenko, O. H. (2020). Expression of and genes in ERN1 knockdown U87 glioma cells: effect of hypoxia and glucose deprivation. Endocrine Regulations, 54(3), 183-195.

Minchenko, D. O., Tsymbal, D. O., Riabovol, O. O., Viletska, Y. M., Lahanovska, Y. O., Sliusar, M. Y., ... & Minchenko, O. H. (2019). Hypoxic regulation of EDN1, EDNRA, EDNRB, and ECE1 gene expressions in ERN1 knockdown U87 glioma cells. Endocrine regulations, 53(4), 250-262.

Chaurasia, M., Gupta, S., Das, A., Dwarakanath, B. S., Simonsen, A., & Sharma, K. (2019). Radiation induces EIF2AK3/PERK and ERN1/IRE1 mediated pro-survival autophagy. Autophagy, 15(8), 1391-1406.

Riabovol, O. O., Tsymbal, D. O., Minchenko, D. O., Lebid-Biletska, K. M., Sliusar, M. Y., Rudnytska, O. V., & Minchenko, O. H. (2019). Effect of glucose deprivation on the expression of genes encoding glucocorticoid receptor and some related factors in ERN1-knockdown U87 glioma cells. Endocrine Regulations, 53(4), 237-249.

Zhang, K. (2018). The primary unfolded protein response transducer endoplasmic reticulum-to-nucleus signaling 1 is downregulated in livers of human nonalcoholic steatohepatitis patients. Environmental Disease, 3(4), 80.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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