METL8 rabbit pAb
- Catalog No.:YT8123
- Applications:IHC;WB
- Reactivity:Human;Mouse
- Target:
- METTL8
- Gene Name:
- METTL8
- Protein Name:
- Methyltransferase-like protein 8 (EC 2.1.1.-)
- Human Swiss Prot No:
- Q9H825
- Mouse Gene Id:
- 228019
- Mouse Swiss Prot No:
- A2AUU0
- Immunogen:
- Synthesized peptide derived from human C-ternal METL8
- Specificity:
- This antibody detects endogenous levels of METL8 at Human, Mouse
- Formulation:
- Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.
- Source:
- Polyclonal, Rabbit,IgG
- Dilution:
- WB 1:500-2000 IHC 1:50-200
- Purification:
- The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
- Concentration:
- 1 mg/ml
- Storage Stability:
- -15°C to -25°C/1 year(Do not lower than -25°C)
- Other Name:
- Methyltransferase-like protein 8 (EC 2.1.1.-)
- Molecular Weight(Da):
- 32kD
- Function:
- Mitochondrial S-adenosyl-L-methionine-dependent methyltransferase that mediates N(3)-methylcytidine modification of residue 32 of the tRNA anticodon loop of mitochondrial tRNA(Ser)(UCN) and tRNA(Thr) . N(3)-methylcytidine methylation modification regulates mitochondrial translation efficiency and is required for activity of the respiratory chain . N(3)-methylcytidine methylation of mitochondrial tRNA(Ser)(UCN) requires the formation of N(6)-dimethylallyladenosine(37) (i6A37) by TRIT1 as prerequisite . May also mediate N(3)-methylcytidine modification of mRNAs . The existence of N(3)-methylcytidine modification on mRNAs is however unclear, and additional evidences are required to confirm the role of the N(3)-methylcytidine-specific mRNA methyltransferase activity of METTL8 in vivo .
- Subcellular Location:
- Mitochondrion . Mitochondrial protein: the cytoplasmic or nuclear localization observed by some groups is either the result of an incorrect localization caused by N-terminal tagging that interferes with mitochondrial targeting, or splice isoforms that lack the N-terminal mitochondrial transit sequence. .
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