本公司经销Eph receptor A2+A3+A4，内皮细胞受体蛋白酪氨酸激酶A2+A3+A4抗体，克隆类型为polyclonal，宿主来源是Rabbit，Eph receptor A2+A3+A4内皮细胞受体蛋白酪氨酸激酶A2+A3+A4抗体可应用于WB、elisa、IP、IF、IHC等实验，欢迎垂询订购！

货号：BY-7553R
英文名称：Anti-Eph receptor A2+A3+A4
中文名称：内皮细胞受体蛋白酪氨酸激酶A2+A3+A4抗体
其他名称：名ECK;EPH Receptor A2;EPH Receptor A3;EPH Receptor A4;EPHA2;EPHA3;EPHA4;ETK1;HEK;HEK4;HEK8;SEK;TYRO4.
抗体来源：Rabbit
克隆类型：polyclonal
蛋白分子量：predicted molecular weight: 105-125kDa
纯化方法：affinity purified by Protein A
交叉反应：hu, mo, rat, pig, chk, cow, hrs
产品介绍：Eph receptor A2 is the receptor for members of the ephrin-A family. It binds to ephrin-A1, -A3, -A4 ａnd -A5. Eph receptor A3 is also a receptor for members of the ephrin-A family. It binds to ephrin-A2, -A3, -A4 ａnd -A5 ａnd is thought to play a role in lymphoid function. Eph receptor A4 is a receptor for members of the ephrin-A family. It binds to ephrin-A1, -A4 ａnd -A5. It binds more poorly to ephrin-A2 ａnd -A3. It may play a role in a signal transduction process involved in hindbrain pattern formation.Function : Receptor tyrosine kinase which binds promiscuously membrane-bound ephrin-A family ligands residing on adjacent cells, leading to contact-dependent bidirectional signaling into neighboring cells. The signaling pathway downstream of the receptor is referred to as forward signaling while the signaling pathway downstream of the ephrin ligand is referred to as reverse signaling. Activated by the ligand ephrin-A1/EFNA1 regulates migration, integrin-mediated adhesion, proliferation ａnd differentiation of cells. Regulates cell adhesion ａnd differentiation through DSG1/desmoglein-1 ａnd inhibition of the ERK1/ERK2 （MAPK3/MAPK1, respectively） signaling pathway. May also participate in UV radiation-induced apoptosis ａnd have a ligand-independent stimulatory effect on chemotactic cell migration. During development, may function in distinctive aspects of pattern formation ａnd subsequently in development of several fetal tissues. Involved for instance in angiogenesis, in early hindbrain development ａnd epithelial proliferation ａnd branching morphogenesis during mammary gland development. Engaged by the ligand ephrin-A5/EFNA5 may regulate lens fiber cells shape ａnd interactions ａnd be important for lens transparency development ａnd maintenance. With ephrin-A2/EFNA2 may play a role in bone remodeling through regulation of osteoclastogenesis ａnd osteoblastogenesis.Subunit : Homodimer. Interacts with SLA. Interacts （phosphorylated form） with VAV2, VAV3 ａnd PI3-kinase p85 subunit （PIK3R1, PIK3R2 or PIK3R3）; critical for the EFNA1-induced activation of RAC1 which stimulates cell migration. Interacts with ANKS1A. Interacts with INPPL1; regulates activated EPHA2 endocytosis ａnd degradation. Interacts （inactivated form） with PTK2/FAK1 ａnd interacts （EFNA1 ligand-activated form） with PTPN11; regulates integrin-mediated adhesion. Interacts with ARHGEF16, DOCK4 ａnd ELMO2; mediates ligand-independent activation of RAC1 which stimulates cell migration. Interacts with CLDN4; phosphorylates CLDN4 ａnd may regulate tight junctions. Interacts with ACP1.Subcellular Location : Cell membrane; Single-pass type I membrane protein. Cell projection, ruffle membrane; Single-pass type I membrane protein. Cell projection, lamellipodium membrane; Single-pass type I membrane protein. Cell junction, focal adhesion. Note=Present at regions of cell-cell contacts but also at the leading edge of migrating cells.Tissue Specificity : Expressed in brain ａnd glioma tissue ａnd glioma cell lines （at protein level）. Expressed most highly in tissues that contain a high proportion of epithelial cells, e.g., skin, intestine, lung, ａnd ovary.Post-translational modifications : Autophosphorylates. Phosphorylated on tyrosine upon binding ａnd activation by EFNA1. Phosphorylated residues Tyr-588 ａnd Tyr-594 are required for binding VAV2 ａnd VAV3 while phosphorylated residues Tyr-735 ａnd Tyr-930 are required for binding PI3-kinase p85 subunit （PIK3R1, PIK3R2 or PIK3R3）. These phosphorylated residues are critical for recruitment of VAV2 ａnd VAV3 ａnd PI3-kinase p85 subunit which transduce downstream signaling to activate RAC1 GTPase ａnd cell migration. Phosphorylated at Ser-897 by PKB; serum-induced phosphorylation which targets EPHA2 to the cell leading edge ａnd stimulates cell migration. Phosphorylation by PKB is inhibited by EFNA1-activated EPHA2 which regulates PKB activity via a reciprocal regulatory loop. Dephosphorylated by ACP1.Ubiquitinated by CHIP/STUB1. Ubiquitination is regulated by the HSP90 chaperone ａnd regulates the receptor stability ａnd activity through proteasomal degradation. ANKS1A prevents ubiquitination ａnd degradation.DISEASE : Genetic variations in EPHA2 are the cause of susceptibility to cataract cortical age-related type 2 （ARCC2） [MIM:613020]. A developmental punctate opacity common in the cortex ａnd present in most lenses. The cataract is white or cerulean, increases in number with age, but rarely affects vision. Defects in EPHA2 are the cause of cataract posterior polar type 1 （CTPP1） [MIM:116600]. A subcapsular opacity, usually disk-shaped, located at the back of the lens. It can have a marked effect on visual acuity.Note=Overexpressed in several cancer types ａnd promotes malignancy.Similarity : Belongs to the protein kinase superfamily. Tyr protein kinase family. Ephrin receptor subfamily. Contains 1 Eph LBD （Eph ligand-binding） domain. Contains 2 fibronectin type-III domains. Contains 1 protein kinase domain. Contains 1 SAM （sterile alpha motif） domain.