Anti-eIF2B4 polyclonal antibody (DPABH-20846)

Goat Anti-Human eIF2B4 (aa 190-202) polyclonal antibody for WB Datasheet

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Specifications


Host Species
Goat
Antibody Isotype
IgG
Species Reactivity
Human
Immunogen
Synthetic peptide: C-RKDYGSKVSLFSH, corresponding to internal sequence amino acids 190-202 of Human eIF2B4 (NP_751945.2; NP_001029288.1; NP_056451.3).
Conjugate
Unconjugated

Applications


Application Notes
WB: 0.3 - 1 μg/ml.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
EIF2B4; eukaryotic translation initiation factor 2B, subunit 4 delta, 67kDa; EIF2B; EIF-2B; EIF2Bdelta; translation initiation factor eIF-2B subunit delta
Entrez Gene ID
UniProt ID

Product Background


Gene summary
EIF2B4 (Eukaryotic Translation Initiation Factor 2B Subunit Delta) is a Protein Coding gene. Diseases associated with EIF2B4 include leukoencephalopathy with vanishing white matter and late infantile cach syndrome. Among its related pathways are Gene Expression and Transport to the Golgi and subsequent modification. GO annotations related to this gene include guanyl-nucleotide exchange factor activity and translation initiation factor binding. Eukaryotic initiation factor 2B (EIF2B), which is necessary for protein synthesis, is a GTP exchange factor composed of five different subunits. The protein encoded by this gene is the fourth, or delta, subunit. Defects in this gene are a cause of leukoencephalopathy with vanishing white matter (VWM) and ovarioleukodystrophy. Multiple transcript variants encoding different isoforms have been found for this gene.
Antigen Description
Catalyzes the exchange of eukaryotic initiation factor 2-bound GDP for GTP. Leukodystrophy with vanishing white matter (VWM) [MIM:603896]: A leukodystrophy that occurs mainly in children. Neurological signs include progressive cerebellar ataxia, spasticity, inconstant optic atrophy and relatively preserved mental abilities. The disease is chronic-progressive with, in most individuals, additional episodes of rapid deterioration following febrile infections or minor head trauma. While childhood onset is the most common form of the disorder, some severe forms are apparent at birth. A severe, early-onset form seen among the Cree and Chippewayan populations of Quebec and Manitoba is called Cree leukoencephalopathy. Milder forms may not become evident until adolescence or adulthood. Some females with milder forms of the disease who survive to adolescence exhibit ovarian dysfunction. This variant of the disorder is called ovarioleukodystrophy. Note=The disease is caused by mutations affecting the gene represented in this entry. Translation initiation factor eIF-2B subunit delta is a protein that in humans is encoded by the EIF2B4 gene. 0The function about eIF2B4 antigen include NOT S-methyl-5-thioribose-1-phosphate isomerase activity; contributes_to guanyl-nucleotide exchange factor activity; contributes_to guanyl-nucleotide exchange factor activity; protein binding.
Pathway
Cap-dependent Translation Initiation; Gene Expression; RNA transport; Recycling of eIF2:GDP.

Citations


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References


Leegwater, PAJ; Pronk, JC; et al. Leukoencephalopathy with vanishing white matter: From magnetic resonance imaging pattern to five genes. JOURNAL OF CHILD NEUROLOGY 18:639-645(2003).
Scali, O; Di Perri, C; et al. The spectrum of mutations for the diagnosis of vanishing white matter disease. NEUROLOGICAL SCIENCES 27:271-277(2006).

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