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Rabbit Anti-CYP2U1 Recombinant Antibody (EG902) (CBMAB-EN1073-LY)

The product is antibody recognizes CYP2U1. The antibody EG902 immunoassay techniques such as: WB: 1:500~1:1000 ELISA: 1:20000.
See all CYP2U1 antibodies

Summary

Host Animal
Rabbit
Specificity
Human, Mouse, Rat
Clone
EG902
Antibody Isotype
IgG
Application
WB: 1:500~1:1000 ELISA: 1:20000

Basic Information

Immunogen
The antibody was produced against synthesized peptide derived from internal of human Cytochrome P450 2U1.
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

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

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

Target

Full Name
Cytochrome P450 Family 2 Subfamily U Member 1
Introduction
CYP2U1 (Cytochrome P450 Family 2 Subfamily U Member 1) is a Protein Coding gene. Diseases associated with CYP2U1 include Spastic Paraplegia 56, Autosomal Recessive and Spastic Paraplegia 46, Autosomal Recessive. Among its related pathways are superpathway of tryptophan utilization and Cytochrome P450 - arranged by substrate type. Gene Ontology (GO) annotations related to this gene include iron ion binding and oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen. An important paralog of this gene is CYP2R1.
Entrez Gene ID
Human113612
Mouse71519
Rat310848
UniProt ID
HumanQ7Z449
MouseQ9CX98
RatQ4V8D1
Alternative Names
Cytochrome P450 Family 2 Subfamily U Member 1; Cytochrome P450, Family 2, Subfamily U, Polypeptide 1; Spastic Paraplegia 49; EC 1.14.14.1; Cytochrome P450 2U1; P450TEC; SPG49; SPG56;
Function
A cytochrome P450 monooxygenase involved in the metabolism of arachidonic acid and its conjugates (PubMed:14660610, PubMed:24563460).

Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (CPR; NADPH-ferrihemoprotein reductase) (PubMed:14660610, PubMed:24563460).

Acts as an omega and omega-1 hydroxylase for arachidonic acid and possibly for other long chain fatty acids. May modulate the arachidonic acid signaling pathway and play a role in other fatty acid signaling processes (PubMed:14660610, PubMed:24563460).

May downregulate the biological activities of N-arachidonoyl-serotonin, an endocannabinoid that has anti-nociceptive effects through inhibition of fatty acid amide hydrolase FAAH, TRPV1 receptor and T-type calcium channels. Catalyzes C-2 oxidation of the indole ring of N-arachidonoyl-serotonin forming a less active product 2-oxo-N-arachidonoyl-serotonin (PubMed:24563460).
Biological Process
Exogenous drug catabolic process Source: GO_Central
Omega-hydroxylase P450 pathway Source: UniProtKB
Organic acid metabolic process Source: GO_Central
Xenobiotic metabolic process Source: GO_Central
Cellular Location
Endoplasmic reticulum membrane; Microsome membrane; Mitochondrion inner membrane
Involvement in disease
Spastic paraplegia 56, autosomal recessive (SPG56):
A form of spastic paraplegia, a neurodegenerative disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Rate of progression and the severity of symptoms are quite variable. Initial symptoms may include difficulty with balance, weakness and stiffness in the legs, muscle spasms, and dragging the toes when walking. Complicated forms are recognized by additional variable features including spastic quadriparesis, seizures, dementia, amyotrophy, extrapyramidal disturbance, cerebral or cerebellar atrophy, optic atrophy, and peripheral neuropathy, as well as by extra neurological manifestations. In SPG56, upper limbs are often also affected. Some SPG56 patients may have a subclinical axonal neuropathy.

Pujol, C., Legrand, A., Parodi, L., Thomas, P., Mochel, F., Saracino, D., ... & Stevanin, G. (2021). Implication of folate deficiency in CYP2U1 loss of function. Journal of Experimental Medicine, 218(11), e20210846.

Sharawat, I. K., Panda, P. K., & Dawman, L. (2021). Spastic paraplegia-56 due to a novel CYP2U1 truncating mutation in an Indian boy: A new report and literature review. Journal of Pediatric Neurosciences, 16(1), 71.

El Matri, K., Falfoul, Y., Habibi, I., Chebil, A., Schorderet, D., & El Matri, L. (2021). Macular Dystrophy with Bilateral Macular Telangiectasia Related to the CYP2U1 Pathogenic Variant Assessed with Multimodal Imaging Including OCT-Angiography. Genes, 12(11), 1795.

Akhtar, A., Ch, S. N., & Hussain, M. (2021). In silico computation of functional SNPs of CYP2U1 protein leading to hereditary spastic paraplegia. Informatics in Medicine Unlocked, 24, 100610.

Bibi, F., Efthymiou, S., Bourinaris, T., Tariq, A., Zafar, F., Rana, N., ... & SYNaPS Study Group. (2020). Rare novel CYP2U1 and ZFYVE26 variants identified in two Pakistani families with spastic paraplegia. Journal of the Neurological Sciences, 411, 116669.

Yu, X., Wu, J., Hu, M., Wu, J., Zhu, Q., Yang, Z., ... & Yue, J. (2019). Glutamate affects the CYP1B1-and CYP2U1-mediated hydroxylation of arachidonic acid metabolism via astrocytic mGlu5 receptor. The International Journal of Biochemistry & Cell Biology, 110, 111-121.

Ma, X., Wei, D., Cheng, G., Li, S., Wang, L., Wang, Y., ... & Zan, L. (2018). Bta-miR-130a/b regulates preadipocyte differentiation by targeting PPARG and CYP2U1 in beef cattle. Molecular and cellular probes, 42, 10-17.

Durand, C. M., Dhers, L., Tesson, C., Tessa, A., Fouillen, L., Jacqueré, S., ... & Goizet, C. (2018). CYP2U1 activity is altered by missense mutations in hereditary spastic paraplegia 56. Human Mutation, 39(1), 140-151.

Minase, G., Miyatake, S., Nabatame, S., Arai, H., Koshimizu, E., Mizuguchi, T., ... & Matsumoto, N. (2017). An atypical case of SPG56/CYP2U1-related spastic paraplegia presenting with delayed myelination. Journal of Human Genetics, 62(11), 997-1000.

Iodice, A., Panteghini, C., Spagnoli, C., Salerno, G. G., Frattini, D., Russo, C., ... & Fusco, C. (2017). Long-term follow-up in spastic paraplegia due to SPG56/CYP2U1: age-dependency rather than genetic variability?. Journal of neurology, 264(3), 586-588.

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

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