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Mouse Monoclonal EF-2 antibody [5B6] (STJ98011)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, IF, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; ELISA 1:10000
Recommended protocols: check protocols
Click or hover above images to see image description for EF-2 Monoclonal Antibody.
Check alternative names for the antibodyExpand
EEF2 antibody, EF2 antibody,|EEF 2 antibody|Eef2 antibody|EF-2 antibody|EF2 antibody|EF2_HUMAN antibody|Elongation factor 2 antibody|Eukaryotic translation elongation factor 2 antibody|Polypeptidyl tRNA translocase antibody|SCA26 antibody|Anti-EEF2 antibody (ab33523)
SCBT cat No: sc-13004|sc-166415|sc-166409|sc-25634|sc-390014|sc-13003|
EF-2 Monoclonal Antibody
|Catalogue No.|| |
EF-2 Monoclonal Antibody detects endogenous levels of EF-2 protein.
Purified recombinant fragment of human EF-2 expressed in E Coli
WB, IHC, IF, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; ELISA 1:10000
EF-2 Antibody was tube-contained. Ascitic fluid containing 0.03% sodium azide.
EF-2 Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Elongation factor 2 antibody, EF-2 antibody
|Protein names|| |
Elongation factor 2 , EF-2
|Protein function|| |
Catalyzes the GTP-dependent ribosomal translocation step during translation elongation. During this step, the ribosome changes from the pre-translocational (PRE) to the post-translocational (POST) state as the newly formed A-site-bound peptidyl-tRNA and P-site-bound deacylated tRNA move to the P and E sites, respectively. Catalyzes the coordinated movement of the two tRNA molecules, the mRNA and conformational changes in the ribosome.
|Involvement in disease|| |
Spinocerebellar ataxia 26 (SCA26) [MIM:609306]: A form of spinocerebellar ataxia, a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the TRAFAC class translation factor GTPase superfamily. Classic translation factor GTPase family. EF-G/EF-2 subfamily. / Contains 1 tr-type G (guanine nucleotide-binding) domain.
|Protein post-translational modifications|| |
Phosphorylation by EF-2 kinase completely inactivates EF-2; it requires prior phosphorylation by CDK2 at Ser-595 during mitotic prometaphase. Phosphorylation by CSK promotes SUMOylation, proteolytic cleavage, and nuclear translocation if the C-terminal fragment. / Diphthamide is 2-[3-carboxyamido-3-(trimethyl-ammonio)propyl]histidine. Diphthamide can be ADP-ribosylated by diphtheria toxin and by Pseudomonas exotoxin A, thus arresting protein synthesis (By similarity). / ISGylated. / Proteolytically processed at two sites following phosphorylation by CSK. / SUMOytated following phosphorylation by CSK, promotes proteolytic cleavage.
|Protein cellular localization|| |
Cytoplasm / Nucleus
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St John’s Laboratory Ltd.
|Product type|| |
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