|Application ||WB, IP|
|Calculated MW||159000 Da|
|Application & Usage||Western blotting (1:300 – 1:3000) and Immunoprecipitation. 293T cell lysate can be used as a positive control. However, the optimal concentrations should be determined individually. The antibody recognizes the BLM of human origin. Reactivity to other species has not been tested.|
|Other Names||BS-Bloom Syndrome, DNA Helicase, RECQ-Like, Type 2- RECQ2, RECQL2, RECQL3|
|Formulation||100 µl affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 1% BSA and 0.02% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||BLM Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Participates in DNA replication and repair. Exhibits a magnesium-dependent ATP-dependent DNA-helicase activity that unwinds single- and double-stranded DNA in a 3'-5' direction. 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. Negatively regulates sister chromatid exchange (SCE).|
|Cellular Location||Nucleus. Note=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|
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Provided below are standard protocols that you may find useful for product applications.
Bloom’s syndrome is an autosomal recessive disorder characterized by pre- and post-natal growth deficiencies, sun sensitivity, immunodeficiency and a predisposition to various cancers. The gene responsible for Bloom’s syndrome, BLM, encodes a protein homologous to the RecQ helicase of E. coli and is mutated in most Bloom’s syndrome patients. One characteristic of Bloom’s syndrome is an increased frequency of sister chromatid exchange (SCE). BLM has been shown to unwind G4 DNA, and a failure of this function is thought to be responsible for the increased rate of SCE. BLM is known to be translocated to the nucleus, where its ATPase activity is stimulated by both single- and double-stranded DNA. Mutations in the yeast SGS1, a homolog of BLM, are known to cause mitotic hyperrecombination similiar to that observed in Bloom’s cells.
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