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Mouse Anti-EIF4EBP2 Recombinant Antibody (CBFYE-0726) (CBMAB-E1158-FY)

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
CBFYE-0726
Antibody Isotype
IgG2a, κ
Application
ELISA, WB

Basic Information

Immunogen
EIF4EBP2 (aa61-120) partial recombinant protein.
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal Antibody
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
Buffer
PBS
Preservative
None
Concentration
Batch dependent
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 61-120

Target

Full Name
eukaryotic translation initiation factor 4E binding protein 2
Introduction
This gene encodes a member of the eukaryotic translation initiation factor 4E binding protein family. The gene products of this family bind eIF4E and inhibit translation initiation. However, insulin and other growth factors can release this inhibition via a phosphorylation-dependent disruption of their binding to eIF4E. Regulation of protein production through these gene products have been implicated in cell proliferation, cell differentiation and viral infection.
Entrez Gene ID
UniProt ID
Alternative Names
Eukaryotic Translation Initiation Factor 4E Binding Protein 2; EIF4E-Binding Protein 2; 4E-BP2; Phosphorylated, Heat And Acid Stable Regulated By Insulin Protein II; Eukaryotic Translation Initiation Factor 4E-Binding Protein 2; PHASII; 4EBP2
Research Area
Repressor of translation initiation involved in synaptic plasticity, learning and memory formation (By similarity).

Regulates EIF4E activity by preventing its assembly into the eIF4F complex: hypophosphorylated form of EIF4EBP2 competes with EIF4G1/EIF4G3 and strongly binds to EIF4E, leading to repress translation. In contrast, hyperphosphorylated form dissociates from EIF4E, allowing interaction between EIF4G1/EIF4G3 and EIF4E, leading to initiation of translation (PubMed:25533957).

EIF4EBP2 is enriched in brain and acts as a regulator of synapse activity and neuronal stem cell renewal via its ability to repress translation initiation (By similarity).

Mediates the regulation of protein translation by hormones, growth factors and other stimuli that signal through the MAP kinase and mTORC1 pathways (By similarity).
Biological Process
cAMP-mediated signaling Source: Ensembl
Insulin receptor signaling pathway Source: Ensembl
Memory Source: UniProtKB
Modulation of chemical synaptic transmission Source: UniProtKB
Negative regulation of translational initiation Source: UniProtKB
Regulation of synaptic plasticity Source: UniProtKB
Social behavior Source: UniProtKB
TOR signaling Source: UniProtKB
Translation Source: ProtInc
Cellular Location
Cytoplasm; Postsynapse
PTM
Phosphorylation at Thr-37, Thr-46, Ser-65, Thr-70 and Ser-83 is mediated by MTOR and corresponds to the hyperphosphorylated form: it abolishes binding to EIF4E by inducing folding of intrinsically disordered regions (PubMed:24207126, PubMed:25533957). First phosphorylated at Thr-37 and Thr-46 by MTOR, inducing folding of region encompassing residues from Pro-18 to Arg-62 of into a four-stranded beta-domain that sequesters the helical YXXXXLPhi motif into a partly buried beta-strand, blocking accessibility to EIF4E. Protein phosphorylated at Thr-37 and Thr-46 is however unstable and subsequent phosphorylation at Ser-65, Thr-70 and Ser-83 is required to stabilize the fold, decreasing affinity for EIF4E by a factor of 4000 (PubMed:24207126, PubMed:25533957). Phosphorylated in response to insulin, EGF and PDGF.
Deamidated at Asn-99 and Asn-102 to aspartate (Asp) in brain. Deamidation promotes interaction with RPTOR, subsequent phosphorylation by mTORC1 and increased translation, leading to impair kinetics of excitatory synaptic transmission. Deamidation takes place during postnatal development, when the PI3K-Akt-mTOR signaling is reduced, suggesting it acts as a compensatory mechanism to promote translation despite attenuated PI3K-Akt-mTOR signaling in neuron development. Deamidation converts Asn residues into a mixture of Asp and isoaspartate; interactions with PCMT1 is required to prevent isoaspartate accumulation and convert isoaspartate to Asp.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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