Anti-SEMA4A Magnetic Beads-IP Kit Product Components
Components | Storage |
Anti-SEMA4A Magnetic Beads1,3 | 2-8℃ for 12 months |
NP40 Cell Lysis Buffer2 | -20℃ for 12 months |
5×TBST(pH7.4) | |
1×TBST(pH7.4) | |
ddH2O | |
CD166 Positive Cell Lysate | -20℃ for 12 months |
Alkaline Elution Buffer | 2-8℃ for 12 months |
Acidity Elution Buffer | 2-8℃ for 12 months |
Neutralization Buffer | 2-8℃ for 12 months |
[1] The IP KIT contains anti-SEMA4A magnetic Beads (2 mg/mL) in phosphate buffered saline (PBS, pH 7.4) with sodium azide (0.1%).
[2] Using NP-40 cell lysate buffer in the kit is required,otherwise,the magnetic beads may be precipitated.
[3] Shipping: Magnetic Beads kits are shipped at ambient temperature in which magnetic beads are provided in liquid buffer.
Anti-SEMA4A Magnetic Beads-IP Kit Product Description
The Anti-SEMA4A magnetic Beads, conjugated with Anti-SEMA4A antibody, are used for immuneprecipitation (IP) of SEMA4A proteins which expressed in vitro expression systems. For IP, the beads are added to a sample containing SEMA4A proteins to form a bead-protein complex. The complex is removed from the solution manually using a magnetic separator. The bound SEMA4A proteins are dissociated from the magnetic beads using an elution buffer. Anti-SEMA4A Magnetic Beads-IP Kit Antibody Information
Immunogen
Recombinant Human Semaphorin 4A / SEMA4A / Semaphorin B protein (Catalog#11756-H08H)
Species Reactivity
Human Semaphorin 4A / SEMA4A /
Source
Polyclonal Human Rabbit IgG
Preparation
Produced in rabbits immunized with purified, recombinant Human Semaphorin 4A / SEMA4A / Semaphorin B (rh Semaphorin 4A / SEMA4A / Semaphorin B; Catalog#11756-H08H; NP_071762.2; Met 1-His 683). Semaphorin 4A / SEMA4A / Semaphorin B specific IgG was purified by Human Semaphorin 4A / SEMA4A / Semaphorin B affinity chromatography.
Applications
Immunoprecipitation (IP), Minimum Protein Purification
Anti-SEMA4A Magnetic Beads Immunoprecipitation (IP) Kit Alternative Names
Anti-CORD10ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-RP35ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-SEMABALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-SEMBALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit
SEMA4A Background Information
Semaphorin-4A, also known as Semaphorin-B, SEMA4A, Sema B and SEMAB, is a single-pass type I membrane protein which belongs to the semaphorin family. It inhibits axonal extension by providing local signals to specify territories inaccessible for growing axons. Semaphorin-4A / SEMA4A contains one Ig-like C2-type (immunoglobulin-like) domain, one PSI domain and one Sema domain. Defects in SEMA4A are the cause of retinitis pigmentosa type 35 (RP35) which leads to degeneration of retinal photoreceptor cells. Patients typically have night vision blindness and loss of midperipheral visual field. As their condition progresses, they lose their far peripheral visual field and eventually central vision as well. Defects in SEMA4A are also the cause of cone-rod dystrophy type 1 (CORD1) which are inherited retinal dystrophies belonging to the group of pigmentary retinopathies. CORDs are characterized by retinal pigment deposits visible on fundus examination, predominantly in the macular region, and initial loss of cone photoreceptors followed by rod degeneration. Semaphorins are secreted, transmembrane, and GPI-linked proteins, defined by cysteine-rich semaphorin protein domains, that have important roles in a variety of tissues. Humans have 2 semaphorins, Drosophila has five, and two are known from DNA viruses. Semaphorins are found in nematodes and crustaceans but not in non-animals. They are grouped into eight classes on the basis of phylogenetic tree analyses and the presence of additional protein motifs. Semaphorins have been implicated in diverse developmental processes such as axon guidance during nervous system development and regulation of cell migration.
References
Clark H.F., et al., 2003, Genome Res. 13: 2265-2270. Ota T., et al., 2004,Nat. Genet. 36: 40-45. Neufeld, G. et al., 2005, Front Biosci. 10 : 751-60. Fiore,R. et al., 2005, Mol Cell Biol. 25 (6):2310-9. Abid A., et al., 2006, J. Med. Genet. 43:378-381.