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。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Anti-Mitofusin 2 Picoband Antibody
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Application 
| WB |
|---|---|
| Primary Accession | O95140 |
| Host | Rabbit |
| Reactivity | Human |
| Clonality | Polyclonal |
| Format | Lyophilized |
| Description | Rabbit IgG polyclonal antibody for Mitofusin-2(MFN2) detection. Tested with WB in Human. |
| Reconstitution | Add 0.2ml of distilled water will yield a concentration of 500ug/ml. |
| Gene ID | 9927 |
|---|---|
| Other Names | Mitofusin-2, 3.6.5.-, Transmembrane GTPase MFN2, MFN2, CPRP1, KIAA0214 |
| Calculated MW | 86402 Da |
| Application Details | Western blot, 0.1-0.5 µg/ml, Human |
| Subcellular Localization | Mitochondrion outer membrane ; Multi- pass membrane protein . Colocalizes with BAX during apoptosis. |
| Tissue Specificity | Ubiquitous; expressed at low level. Highly expressed in heart and kidney. . |
| Source | Eukaryota |
| Protein Name | Mitofusin-2 |
| Contents | Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3. |
| Immunogen | E.coli-derived human Mitofusin 2 recombinant protein (Position: V601-R757). Human Mitofusin 2 shares 96% and 95% amino acid (aa) sequence identity with mouse and rat Mitofusin 2, respectively. |
| Purification | Immunogen affinity purified. |
| Cross Reactivity | No cross reactivity with other proteins |
| Storage | At -20˚C for one year. After r˚Constitution, at 4˚C for one month. It˚Can also be aliquotted and stored frozen at -20˚C for a longer time.Avoid repeated freezing and thawing. |
| Sequence Similarities | Belongs to the TRAFAC class dynamin-like GTPase superfamily. Dynamin/Fzo/YdjA family. Mitofusin subfamily. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | MFN2 {ECO:0000303|PubMed:12598526, ECO:0000312|HGNC:HGNC:16877} |
|---|---|
| Function | Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:11181170, PubMed:11950885, PubMed:19889647, PubMed:26214738, PubMed:28114303). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events (PubMed:28114303). Overexpression induces the formation of mitochondrial networks (PubMed:28114303). Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (Probable). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes (By similarity). Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy) (PubMed:23620051). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (By similarity). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (By similarity). |
| Cellular Location | Mitochondrion outer membrane; Multi-pass membrane protein Note=Colocalizes with BAX during apoptosis |
| Tissue Location | Ubiquitous; expressed at low level. Highly expressed in heart and kidney. |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Mitofusin-2 is a protein that in humans is encoded by the MFN2 gene. It is mapped to chromosome 1 and encodes a 757-amino acid protein that contains an ATP/GTP-binding site motif. This gene is expressed in many tissues and cell lines such as brain and KG-1 with the highest expression in heart and skeletal muscle. It has been found that MFN2 triggers mitochondrial energization, at least in part, by regulating OXPHOS expression through signals that are independent of its role as a mitochondrial fusion protein. And it contributes to the maintenance and operation of the mitochondrial network. Axonal CMT type 2A and autosomal dominant HMSN VI are caused by MFN2 and mutations in MFN2, which emphasizes its important role of mitochondrial function for both optic atrophies and peripheral neuropathies.
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