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Mouse Anti-FTO Monoclonal Antibody (5-2H10) (CBMAB-1285-YC)

Provided herein is a mouse monoclonal antibody against Human FTO. The antibody, clone 5-2H10, can be used for immunoassay techniques, such as FC, ICC, IF and WB.
See all FTO antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
5-2H10
Antibody Isotype
IgG2a
Application
FC, ICC, IF, WB

Basic Information

Immunogen
Synthetic peptide from Human FTO
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG2a
Clonality
Monoclonal
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%, as determined by SDS-PAGE analysis
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
FTO, Alpha-Ketoglutarate Dependent Dioxygenase
Introduction
FTO is a nuclear protein of the AlkB related non-haem iron and 2-oxoglutarate-dependent oxygenase superfamily. Studies in mice and humans indicate a role in nervous and cardiovascular systems and a strong association with body mass index, obesity risk, and type 2 diabetes.
Entrez Gene ID
Human79068
Mouse26383
Rat291905
UniProt ID
HumanQ9C0B1
MouseQ8BGW1
RatQ2A121
Alternative Names
GDFD; ALKBH9; BMIQ14
Function
RNA demethylase that mediates oxidative demethylation of different RNA species, such as mRNAs, tRNAs and snRNAs, and acts as a regulator of fat mass, adipogenesis and energy homeostasis (PubMed:22002720, PubMed:26458103, PubMed:28002401, PubMed:30197295, PubMed:26457839, PubMed:25452335).

Specifically demethylates N6-methyladenosine (m6A) RNA, the most prevalent internal modification of messenger RNA (mRNA) in higher eukaryotes (PubMed:22002720, PubMed:26458103, PubMed:30197295, PubMed:26457839, PubMed:25452335).

M6A demethylation by FTO affects mRNA expression and stability (PubMed:30197295).

Also able to demethylate m6A in U6 small nuclear RNA (snRNA) (PubMed:30197295).

Mediates demethylation of N6,2'-O-dimethyladenosine cap (m6A(m)), by demethylating the N6-methyladenosine at the second transcribed position of mRNAs and U6 snRNA (PubMed:28002401, PubMed:30197295).

Demethylation of m6A(m) in the 5'-cap by FTO affects mRNA stability by promoting susceptibility to decapping (PubMed:28002401).

Also acts as a tRNA demethylase by removing N1-methyladenine from various tRNAs (PubMed:30197295).

Has no activity towards 1-methylguanine (PubMed:20376003).

Has no detectable activity towards double-stranded DNA (PubMed:20376003).

Also able to repair alkylated DNA and RNA by oxidative demethylation: demethylates single-stranded RNA containing 3-methyluracil, single-stranded DNA containing 3-methylthymine and has low demethylase activity towards single-stranded DNA containing 1-methyladenine or 3-methylcytosine (PubMed:18775698, PubMed:20376003).

Ability to repair alkylated DNA and RNA is however unsure in vivo (PubMed:18775698, PubMed:20376003).

Involved in the regulation of fat mass, adipogenesis and body weight, thereby contributing to the regulation of body size and body fat accumulation (PubMed:18775698, PubMed:20376003).

Involved in the regulation of thermogenesis and the control of adipocyte differentiation into brown or white fat cells (PubMed:26287746).

Regulates activity of the dopaminergic midbrain circuitry via its ability to demethylate m6A in mRNAs (By similarity).

Plays an oncogenic role in a number of acute myeloid leukemias by enhancing leukemic oncogene-mediated cell transformation: acts by mediating m6A demethylation of target transcripts such as MYC, CEBPA, ASB2 and RARA, leading to promote their expression (PubMed:28017614, PubMed:29249359).
Biological Process
Adipose tissue development Source: Ensembl
DNA dealkylation involved in DNA repair Source: UniProtKB
DNA demethylation Source: BHF-UCL
mRNA destabilization Source: UniProtKB
Oxidative demethylation Source: BHF-UCL
Oxidative single-stranded DNA demethylation Source: UniProtKB
Oxidative single-stranded RNA demethylation Source: UniProtKB
Regulation of brown fat cell differentiation Source: UniProtKB
Regulation of lipid storage Source: UniProtKB
Regulation of multicellular organism growth Source: Ensembl
Regulation of respiratory system process Source: Ensembl
Regulation of white fat cell proliferation Source: Ensembl
RNA repair Source: BHF-UCL
Temperature homeostasis Source: Ensembl
Cellular Location
Nucleus; Nucleus speckle; Cytoplasm. Localizes mainly in the nucleus, where it is able to demethylate N6-methyladenosine (m6A) and N6,2'-O-dimethyladenosine cap (m6A(m)) in U6 small nuclear RNA (snRNA), N1-methyladenine from tRNAs and internal m6A in mRNAs (PubMed:30197295). In the cytoplasm, mediates demethylation of m6A and m6A(m) in mRNAs and N1-methyladenine from tRNAs (PubMed:30197295).
Involvement in disease
Growth retardation, developmental delay, and facial dysmorphism (GDFD):
A severe polymalformation syndrome characterized by postnatal growth retardation, microcephaly, severe psychomotor delay, functional brain deficits and characteristic facial dysmorphism. In some patients, structural brain malformations, cardiac defects, genital anomalies, and cleft palate are observed. Early death occurs by the age of 3 years.
Obesity (OBESITY):
Disease susceptibility is associated with variants affecting the gene represented in this entry. It is unclear whether variations associated with obesity directly affect FTO function or alter the expression of adjacent genes such as IRX3, rather than FTO itself (PubMed:24646999, PubMed:26287746). A pathogenic intronic FTO variation (rs1421085) disrupts an evolutionarily conserved motif for ARID5B binding (PubMed:26287746). Loss of ARID5B binding results in overexpression of two genes distal to FTO, IRX3 and IRX5. IRX3 and IRX5 overexpression shifts pre-adipocytes differentiation from brown to white fat cells, resulting in increased lipid storage and loss of mitochondrial thermogenesis (PubMed:26287746). A condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.

Li, S., & Cao, L. (2022). Demethyltransferase FTO alpha-ketoglutarate dependent dioxygenase (FTO) regulates the proliferation, migration, invasion and tumor growth of prostate cancer by modulating the expression of melanocortin 4 receptor (MC4R). Bioengineered, 13(3), 5598-5612.

Sommerkamp, P. (2022). Substrates of the m6A demethylase FTO: FTO-LINE1 RNA axis regulates chromatin state in mESCs. Signal Transduction and Targeted Therapy, 7(1), 212.

Wang, D., Li, Y., Xu, X., Zhao, S., Wang, Z., Yang, J., ... & Liu, M. (2022). FTO knockdown alleviates hypoxia-induced PC12 cell injury by stabilizing GADD45B in an IGF2BP2-dependent manner. Biochemical and Biophysical Research Communications, 619, 166-172.

Yi, W., Yu, Y., Li, Y., Yang, J., Gao, S., & Xu, L. (2021). The tumor-suppressive effects of alpha-ketoglutarate-dependent dioxygenase FTO via N6-methyladenosine RNA methylation on bladder cancer patients. Bioengineered, 12(1), 5323-5333.

Czogała, W., Czogała, M., Strojny, W., Wątor, G., Wołkow, P., Wójcik, M., ... & Skoczeń, S. (2021). Methylation and expression of FTO and PLAG1 genes in childhood obesity: Insight into anthropometric parameters and glucose–lipid metabolism. Nutrients, 13(5), 1683.

Czogała, W., Strojny, W., Schab, M., Grabowska, A., Miklusiak, K., Kowalczyk, W., ... & Skoczeń, S. (2021). FTO and PLAG1 genes expression and FTO methylation predict changes in circulating levels of adipokines and gastrointestinal peptides in children. Nutrients, 13(10), 3585.

Marcinkowski, M., Pilžys, T., Garbicz, D., Steciuk, J., Zugaj, D., Mielecki, D., ... & Grzesiuk, E. (2020). Human and Arabidopsis alpha‐ketoglutarate‐dependent dioxygenase homolog proteins—New players in important regulatory processes. IUBMB life, 72(6), 1126-1144.

Kucher, A. N. (2020). The FTO Gene and Diseases: The role of genetic polymorphism, epigenetic modifications, and environmental factors. Russian Journal of Genetics, 56, 1025-1043.

Wakisaka, K. T., Muraoka, Y., Shimizu, J., Yamaguchi, M., Ueoka, I., Mizuta, I., ... & Yamaguchi, M. (2019). Drosophila alpha-ketoglutarate-dependent dioxygenase AlkB is involved in repair from neuronal disorders induced by ultraviolet damage. NeuroReport, 30(15), 1039-1047.

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

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