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Mouse Anti-HBS1L (AA 1-260) Recombinant Antibody (CBFYH-0756) (CBMAB-H1661-FY)

This product is mouse antibody that recognizes HBS1L. The antibody CBFYH-0756 can be used for immunoassay techniques such as: WB.
See all HBS1L antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYH-0756
Antibody Isotype
IgG1
Application
WB

Basic Information

Immunogen
Human recombinant protein fragment corresponding to amino acids 1-260 of human HBS1L produced in E. coli
Specificity
Human
Antibody Isotype
IgG1
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
Concentration
9.31 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 1-260

Target

Full Name
Hbs1-like (S. cerevisiae)
Introduction
This gene encodes a member of the GTP-binding elongation factor family. It is expressed in multiple tissues with the highest expression in heart and skeletal muscle. The intergenic region of this gene and the MYB gene has been identified to be a quantitative trait locus (QTL) controlling fetal hemoglobin level, and this region influnces erythrocyte, platelet, and monocyte counts as well as erythrocyte volume and hemoglobin content. DNA polymorphisms at this region associate with fetal hemoglobin levels and pain crises in sickle cell disease. A single nucleotide polymorphism in exon 1 of this gene is significantly associated with severity in beta-thalassemia/Hemoglobin E. Multiple alternatively spliced transcript variants encoding different protein isoforms have been found for this gene.
Entrez Gene ID
10767
UniProt ID
Q9Y450
Alternative Names
HBS1 Like Translational GTPase; ERF3 Family Member; ERFS; HBS1; Hsp70 Subfamily B Suppressor 1-Like Protein; HBS1-Like Translational GTPase; HBS1 (S. Cerevisiae)-Like; HBS1-Like (S. Cerevisiae)
Function
Cotranslational quality control factor involved in the No-Go Decay (NGD) pathway (PubMed:21448132).

In the presence of ABCE1 and PELO, is required for 48S complex formation from 80S ribosomes and dissociation of vacant 80S ribosomes (PubMed:21448132).

Together with PELO and in presence of ABCE1, recognizes stalled ribosomes and promotes dissociation of elongation complexes assembled on non-stop mRNAs; this triggers endonucleolytic cleavage of the mRNA, a mechanism to release non-functional ribosomes and to degrade damaged mRNAs as part of the No-Go Decay (NGD) pathway (PubMed:21448132).

Isoform 2:
Facilitates the association of the exosome complex with the SKI complex.
Biological Process
Signal transduction Source: ProtInc
Translation Source: GO_Central
Cellular Location
Isoform 2: Cytoplasm

Chumchuen, S., Sripichai, O., Jearawiriyapaisarn, N., Fucharoen, S., & Peerapittayamongkol, C. (2023). Induction of fetal hemoglobin: Lentiviral shRNA knockdown of HBS1L in β0-thalassemia/HbE erythroid cells. Plos one, 18(3), e0281059.

Sales, R. R., Nogueira, B. L., Belisário, A. R., Faria, G., Mendes, F., Viana, M. B., & Luizon, M. R. (2022). Fetal hemoglobin-boosting haplotypes of BCL11A gene and HBS1L-MYB intergenic region in the prediction of clinical and hematological outcomes in a cohort of children with sickle cell anemia. Journal of Human Genetics, 67(12), 701-709.

Mohammad, S. N. N. A. I., Iberahim, S., Wan Ab Rahman, W. S., Hassan, M. N., Edinur, H. A., Azlan, M., & Zulkafli, Z. (2022). Single Nucleotide Polymorphisms in XMN1-HBG2, HBS1L-MYB, and BCL11A and Their Relation to High Fetal Hemoglobin Levels That Alleviate Anemia. Diagnostics, 12(6), 1374.

Bashir, S., Mahmood, S., Mohsin, S., Tabassum, I., Ghafoor, M., & Sajjad, O. (2021). Modulatory effect of single nucleotide polymorphism in Xmn1, BCL11A and HBS1L-MYB loci on foetal haemoglobin levels in β-thalassemia major and Intermedia patients. J. Pak. Med. Assoc, 71, 1394-1398.

Akbulut-Jeradi, N., Fernandez, M. J., Al Khaldi, R., Sukumaran, J., & Adekile, A. (2021). Unique polymorphisms at BCL11A, HBS1L-MYB and HBB loci associated with HbF in Kuwaiti patients with sickle cell disease. Journal of personalized medicine, 11(6), 567.

Sales, R. R., Belisário, A. R., Faria, G., Mendes, F., Luizon, M. R., & Viana, M. B. (2020). Functional polymorphisms of BCL11A and HBS1L-MYB genes affect both fetal hemoglobin level and clinical outcomes in a cohort of children with sickle cell anemia. Annals of Hematology, 99(7), 1453-1463.

Yang, K., Wu, Y., Ma, Y., Xiao, J., Zhou, Y., & Yin, X. (2020). The association of HBG2, BCL11A, and HBS1L-MYB polymorphisms to thalidomide response in Chinese β-thalassemia patients. Blood Cells, Molecules, and Diseases, 84, 102442.

O’Connell, A. E., Gerashchenko, M. V., O’Donohue, M. F., Rosen, S. M., Huntzinger, E., Gleeson, D., ... & Agrawal, P. B. (2019). Mammalian Hbs1L deficiency causes congenital anomalies and developmental delay associated with Pelota depletion and 80S monosome accumulation. PLoS genetics, 15(2), e1007917.

Morrison, T. A., Wilcox, I., Luo, H. Y., Farrell, J. J., Kurita, R., Nakamura, Y., ... & Chui, D. H. (2018). A long noncoding RNA from the HBS1L-MYB intergenic region on chr6q23 regulates human fetal hemoglobin expression. Blood Cells, Molecules, and Diseases, 69, 1-9.

Trifa, A. P., Bănescu, C., Bojan, A. S., Voina, C. M., Popa, Ș., Vișan, S., ... & Popp, R. A. (2018). MECOM, HBS1L‐MYB, THRB‐RARB, JAK2, and TERT polymorphisms defining the genetic predisposition to myeloproliferative neoplasms: a study on 939 patients. American Journal of Hematology, 93(1), 100-106.

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

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