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Mouse Anti-BLM Recombinant Antibody (1E4) (CBMAB-A0797-LY)

The product is antibody recognizes BLM. The antibody 1E4 immunoassay techniques such as: WB, ELISA.
See all BLM antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
1E4
Antibody Isotype
IgG1, κ
Application
WB, ELISA

Basic Information

Immunogen
BLM (NP_000048, 1196 a.a. ~ 1295 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Specificity
Human
Antibody Isotype
IgG1, κ
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
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.

Target

Full Name
Bloom Syndrome RecQ Like Helicase
Introduction
The Bloom syndrome gene product is related to the RecQ subset of DExH box-containing DNA helicases and has both DNA-stimulated ATPase and ATP-dependent DNA helicase activities. Mutations causing Bloom syndrome delete or alter helicase motifs and may disable the 3'-5' helicase activity. The normal protein may act to suppress inappropriate recombination. [provided by RefSeq]
Entrez Gene ID
641
UniProt ID
P54132
Alternative Names
BS; MGC126616; MGC131618; MGC131620; RECQ2; RECQL2; RECQL3
Function
ATP-dependent DNA helicase that unwinds single- and double-stranded DNA in a 3'-5' direction (PubMed:9388193, PubMed:24816114, PubMed:25901030).
Participates in DNA replication and repair (PubMed:12019152, PubMed:21325134, PubMed:23509288).
Involved in 5'-end resection of DNA during double-strand break (DSB) repair: unwinds DNA and recruits DNA2 which mediates the cleavage of 5'-ssDNA (PubMed:21325134).
Negatively regulates sister chromatid exchange (SCE) (PubMed:25901030).
Stimulates DNA 4-way junction branch migration and DNA Holliday junction dissolution (PubMed:25901030).
Binds single-stranded DNA (ssDNA), forked duplex DNA and DNA Holliday junction (PubMed:20639533, PubMed:24257077, PubMed:25901030).
Recruited by the KHDC3L-OOEP scaffold to DNA replication forks where it is retained by TRIM25 ubiquitination, it thereby promotes the restart of stalled replication forks (By similarity).
Biological Process
Cellular response to camptothecin Source: UniProtKB
Cellular response to DNA damage stimulus Source: UniProtKB
Cellular response to hydroxyurea Source: UniProtKB
Cellular response to ionizing radiation Source: UniProtKB
DNA double-strand break processing Source: UniProtKB
DNA duplex unwinding Source: UniProtKB
DNA recombination Source: GO_Central
DNA repair Source: GO_Central
DNA replication Source: BHF-UCL
DNA unwinding involved in DNA replication Source: GO_Central
Double-strand break repair via homologous recombination Source: GO_Central
G-quadruplex DNA unwinding Source: BHF-UCL
Mitotic G2 DNA damage checkpoint Source: UniProtKB
Negative regulation of cell division Source: UniProtKB
Negative regulation of DNA recombination Source: UniProtKB
Positive regulation of transcription, DNA-templated Source: UniProtKB
Protein complex oligomerization Source: UniProtKB
Protein homooligomerization Source: UniProtKB
Regulation of cyclin-dependent protein serine/threonine kinase activity Source: UniProtKB
Regulation of DNA-dependent DNA replication Source: UniProtKB
Regulation of signal transduction by p53 class mediator Source: Reactome
Replication fork processing Source: UniProtKB
Replication fork protection Source: UniProtKB
Response to X-ray Source: UniProtKB
T-circle formation Source: BHF-UCL
Telomere maintenance Source: GO_Central
Telomere maintenance via semi-conservative replication Source: Reactome
Telomeric D-loop disassembly Source: BHF-UCL
Cellular Location
Nucleus. Together with SPIDR, is redistributed in discrete nuclear DNA damage-induced foci following hydroxyurea (HU) or camptothecin (CPT) treatment. Accumulated at sites of DNA damage in a RMI complex- and SPIDR-dependent manner.
Involvement in disease
Bloom syndrome (BLM): An autosomal recessive disorder. It is characterized by proportionate pre- and postnatal growth deficiency, sun-sensitive telangiectatic hypo- and hyperpigmented skin, predisposition to malignancy, and chromosomal instability.
PTM
Poly-ubiquitinated by TRIM25 at Lys-259.
Phosphorylated in response to DNA damage. Phosphorylation requires the FANCA-FANCC-FANCE-FANCF-FANCG protein complex, as well as the presence of RMI1.

Zhu, M., Wu, W., Togashi, Y., Liang, W., Miyoshi, Y., & Ohta, T. (2021). HERC2 inactivation abrogates nucleolar localization of RecQ helicases BLM and WRN. Scientific reports, 11(1), 1-13.

Kaur, E., Agrawal, R., & Sengupta, S. (2021). Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?. Frontiers in Genetics, 12, 277.

Grigaitis, R., Ranjha, L., Wild, P., Kasaciunaite, K., Ceppi, I., Kissling, V., ... & Matos, J. (2020). Phosphorylation of the RecQ helicase Sgs1/BLM controls its DNA unwinding activity during meiosis and mitosis. Developmental Cell, 53(6), 706-723.

Tan, J., Wang, X., Phoon, L., Yang, H., & Lan, L. (2020). Resolution of ROS‐induced G‐quadruplexes and R‐loops at transcriptionally active sites is dependent on BLM helicase. FEBS letters, 594(9), 1359-1367.

Zhu, X., Chen, H., Yang, Y., Xu, C., Zhou, J., Zhou, J., & Chen, Y. (2018). Distinct prognosis of mRNA expression of the five RecQ DNA-helicase family members–RECQL, BLM, WRN, RECQL4, and RECQL5–in patients with breast cancer. Cancer management and research, 10, 6649.

Qian, X., Feng, S., Xie, D., Feng, D., Jiang, Y., & Zhang, X. (2017). RecQ helicase BLM regulates prostate cancer cell proliferation and apoptosis. Oncology letters, 14(4), 4206-4212.

Chang, E. Y. C., Novoa, C. A., Aristizabal, M. J., Coulombe, Y., Segovia, R., Chaturvedi, R., ... & Stirling, P. C. (2017). RECQ-like helicases Sgs1 and BLM regulate R-loop–associated genome instability. Journal of Cell Biology, 216(12), 3991-4005.

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

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