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Mouse Anti-FANCM Recombinant Antibody (CV5.1) (CBMAB-F0056-CQ)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CV5.1
Antibody Isotype
IgG1, κ
Application
WB, IF, IP

Basic Information

Immunogen
His-tagged denatured FANCM (aa 1507-1679) made in E. coli
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
Concentration
1 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.

Target

Full Name
Fanconi Anemia Complementation Group M
Introduction
The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ (also called BRIP1), FANCL, FANCM and FANCN (also called PALB2). The previously defined group FANCH is the same as FANCA. Fanconi anemia is a genetically heterogeneous recessive disorder characterized by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and defective DNA repair. The members of the Fanconi anemia complementation group do not share sequence similarity; they are related by their assembly into a common nuclear protein complex. This gene encodes the protein for complementation group M. Alternative splicing results in multiple transcript variants.
Entrez Gene ID
57697
UniProt ID
Q8IYD8
Alternative Names
Fanconi Anemia Complementation Group M; KIAA1596; Fanconi Anemia-Associated Polypeptide Of 250 KDa; ATP-Dependent RNA Helicase FANCM; Protein Hef Ortholog; FAAP250;
Research Area
DNA-dependent ATPase component of the Fanconi anemia (FA) core complex (PubMed:16116422).

Required for the normal activation of the FA pathway, leading to monoubiquitination of the FANCI-FANCD2 complex in response to DNA damage, cellular resistance to DNA cross-linking drugs, and prevention of chromosomal breakage (PubMed:16116422, PubMed:19423727, PubMed:20347428, PubMed:20347429, PubMed:29231814).

In complex with CENPS and CENPX, binds double-stranded DNA (dsDNA), fork-structured DNA (fsDNA) and Holliday junction substrates (PubMed:20347428, PubMed:20347429).

Its ATP-dependent DNA branch migration activity can process branched DNA structures such as a movable replication fork. This activity is strongly stimulated in the presence of CENPS and CENPX (PubMed:20347429).

In complex with FAAP24, efficiently binds to single-strand DNA (ssDNA), splayed-arm DNA, and 3'-flap substrates (PubMed:17289582).

In vitro, on its own, strongly binds ssDNA oligomers and weakly fsDNA, but does not bind to dsDNA (PubMed:16116434).
Biological Process
Double-strand break repair via synthesis-dependent strand annealing Source: GO_Central
Interstrand cross-link repair Source: GO_Central
Positive regulation of protein monoubiquitination Source: UniProtKB
Replication fork processing Source: UniProtKB
Replication fork reversal Source: GO_Central
Resolution of meiotic recombination intermediates Source: UniProtKB
Cellular Location
Nucleus
Involvement in disease
Spermatogenic failure 28 (SPGF28):
An autosomal recessive infertility disorder caused by spermatogenesis defects that result in oligoasthenospermia or non-obstructive azoospermia.
Premature ovarian failure 15 (POF15):
An ovarian disorder defined as the cessation of ovarian function under the age of 40 years. It is characterized by oligomenorrhea or amenorrhea, in the presence of elevated levels of serum gonadotropins and low estradiol.
PTM
Phosphorylated; hyperphosphorylated in response to genotoxic stress.
More Infomation

Desjardins, S. D., Simmonds, J., Guterman, I., Kanyuka, K., Burridge, A. J., Tock, A. J., ... & Higgins, J. D. (2022). FANCM promotes class I interfering crossovers and suppresses class II non-interfering crossovers in wheat meiosis. Nature communications, 13(1), 1-12.

Panday, A., Willis, N. A., Elango, R., Menghi, F., Duffey, E. E., Liu, E. T., & Scully, R. (2021). FANCM regulates repair pathway choice at stalled replication forks. Molecular cell, 81(11), 2428-2444.

Zhang, J., Bellani, M. A., James, R. C., Pokharel, D., Zhang, Y., Reynolds, J. J., ... & Seidman, M. M. (2020). DONSON and FANCM associate with different replisomes distinguished by replication timing and chromatin domain. Nature communications, 11(1), 1-15.

Pan, X., Chen, Y., Biju, B., Ahmed, N., Kong, J., Goldenberg, M., ... & Zhang, D. (2019). FANCM suppresses DNA replication stress at ALT telomeres by disrupting TERRA R-loops. Scientific reports, 9(1), 1-14.

Basbous, J., & Constantinou, A. (2019). A tumor suppressive DNA translocase named FANCM. Critical Reviews in Biochemistry and Molecular Biology, 54(1), 27-40.

Yin, H., Ma, H., Hussain, S., Zhang, H., Xie, X., Jiang, L., ... & Shi, Q. (2019). A homozygous FANCM frameshift pathogenic variant causes male infertility. Genetics in Medicine, 21(1), 62-70.

Domingues-Silva, B., Silva, B., & Azzalin, C. M. (2019). ALTernative functions for human FANCM at telomeres. Frontiers in Molecular Biosciences, 6, 84.

Lu, R., O’Rourke, J. J., Sobinoff, A. P., Allen, J. A., Nelson, C. B., Tomlinson, C. G., ... & Pickett, H. A. (2019). The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT). Nature communications, 10(1), 1-14.

Silva, B., Pentz, R., Figueira, A. M., Arora, R., Lee, Y. W., Hodson, C., ... & Azzalin, C. M. (2019). FANCM limits ALT activity by restricting telomeric replication stress induced by deregulated BLM and R-loops. Nature communications, 10(1), 1-16.

Wang, H., Li, S., Oaks, J., Ren, J., Li, L., & Wu, X. (2018). The concerted roles of FANCM and Rad52 in the protection of common fragile sites. Nature communications, 9(1), 1-14.

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

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