癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
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Agrin Rabbit pAb
Agrin Rabbit pAb
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- 背景知识
Application 
| IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | O00468 |
| Reactivity | Mouse |
| Predicted | Human, Sheep |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 217320 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human Agrin |
| Epitope Specificity | 1151-1245/2045 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Secreted, extracellular space, extracellular matrix. Note=Synaptic basal lamina at the neuromuscular junction. |
| SIMILARITY | Contains 4 EGF-like domains.Contains 9 Kazal-like domains. Contains 2 laminin EGF-like domains. Contains 3 laminin G-like domains. Contains 1 NtA (N-terminal agrin) domain. Contains 1 SEA domain. |
| SUBUNIT | Interacts with LRP4; the interaction is direct and recruits AGRIN to the MUSK signaling complex composed at least of MUSK and LRP4 (By similarity). Binds to laminin. |
| Post-translational modifications | Contains heparan sulfate chains as well as N-linked and O-linked oligosaccharides. 0-fucosylation of EGF repeat 4 of muscle AGRN by POFUT1 prevents its ability to form AChR clusters. |
| DISEASE | Defects in AGRN are a cause of myasthenia, limb-girdle, familial (LGM) [MIM:254300]. A congenital myasthenic syndrome characterized by a typical 'limb girdle' pattern of muscle weakness with small, simplified neuromuscular junctions but normal acetylcholine receptor and acetylcholinesterase function. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | This gene encodes one of several proteins that are critical in the development of the neuromuscular junction (NMJ), as identified in mouse knock-out studies. The encoded protein contains several laminin G, Kazal type serine protease inhibitor, and epidermal growth factor domains. Additional post-translational modifications occur to add glycosaminoglycans and disulfide bonds. In one family with congenital myasthenic syndrome affecting limb-girdle muscles, a mutation in this gene was found. [provided by RefSeq, Aug 2011]. |
| Gene ID | 375790 |
|---|---|
| Other Names | Agrin, Agrin N-terminal 110 kDa subunit, Agrin C-terminal 110 kDa subunit, Agrin C-terminal 90 kDa fragment, C90, Agrin C-terminal 22 kDa fragment, C22, AGRN, AGRIN |
| Target/Specificity | Detected on the aortic endothelium (at protein level). |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500 |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | AGRN |
|---|---|
| Synonyms | AGRIN |
| Function | Depending on alternative splicing and post-translational modifications, it has a role in different processes, including neuromuscular junction formation and maintenance, and regulation of neurite outgrowth (By similarity). Also involved in positive regulation of cartilage formation through alpha-dystroglycan binding and up- regulation of SOX9 (PubMed:26290588). |
| Cellular Location | [Isoform 1]: Secreted, extracellular space, extracellular matrix. Note=Synaptic basal lamina at the neuromuscular junction. {ECO:0000250|UniProtKB:P31696} |
| Tissue Location | Expressed in basement membranes of lung and kidney. Muscle- and neuron-specific isoforms are found. Isoforms (y+) with the 4 AA insert and (z+8) isoforms with the 8 AA insert are all neuron- specific. Isoforms (z+11) are found in both neuronal and non-neuronal tissues. |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
This gene encodes one of several proteins that are critical in the development of the neuromuscular junction (NMJ), as identified in mouse knock-out studies. The encoded protein contains several laminin G, Kazal type serine protease inhibitor, and epidermal growth factor domains. Additional post-translational modifications occur to add glycosaminoglycans and disulfide bonds. In one family with congenital myasthenic syndrome affecting limb-girdle muscles, a mutation in this gene was found. [provided by RefSeq, Aug 2011].
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