EphA3 polyclonal (N-term), anti-human

EphA3 polyclonal (N-term), anti-human

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In stock
SKU
AC-AP7608a
Catalog Number: AC-AP7608a
Size: 80 µl, 400 µl
Isotype: Rabbit IgG
Clone Name: RB01584
Applications: IHC-P, WB
Datasheet

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Background:
Protein kinases are enzymes that transfer a phosphate group from a phosphate donor, generally the g phosphate of ATP, onto an acceptor amino acid in a substrate protein. By this basic mechanism, protein kinases mediate most of the signal transduction in eukaryotic cells, regulating cellular metabolism, transcription, cell cycle progression, cytoskeletal rearrangement and cell movement, apoptosis, and differentiation. With more than 500 gene products, the protein kinase family is one of the largest families of proteins in eukaryotes. The family has been classified in 8 major groups based on sequence comparison of their tyrosine (PTK) or serine/threonine (STK) kinase catalytic domains. The tyrosine kinase (TK) group is mainly involved in the regulation of cell-cell interactions such as differentiation, adhesion, motility and death. There are currently about 90 TK genes sequenced, 58 are of receptor protein TK (e.g. EGFR, EPH, FGFR, PDGFR, TRK, and VEGFR families), and 32 of cytosolic TK (e.g. ABL, FAK, JAK, and SRC families).

Other Names:
Ephrin type-A receptor 3, EPH-like kinase 4, EK4, hEK4, HEK, Human embryo kinase, Tyrosine-protein kinase TYRO4, Tyrosine-protein kinase receptor ETK1, Eph-like tyrosine kinase 1, EPHA3, ETK, ETK1, HEK, TYRO4

Target/Specificity:
This EphA3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 115-144 amino acids from the N-terminal region of human EphA3.

Antigen Region:
115-144

Antigen Type: Synthetic Peptide

Gene Name: EPHA3
Gene ID: 2042
Primary Accession: P29320
NCBI Accession: NP_005224.2;NP_872585.1
Other Accession: P29319
Format: Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
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