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。
ATL1 Antibody (C-term) 精选
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | Q8WXF7 |
| Other Accession | Q6PST4, Q8BH66, Q60HD2, Q58D72, NP_001121185.1, NP_056999.2 |
| Reactivity | Human |
| Predicted | Bovine, Monkey, Mouse, Rat, Canine, Rabbit, Chicken |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 63544 Da |
| Antigen Region | 477-504 aa |
| Gene ID | 51062 |
|---|---|
| Other Names | Atlastin-1, 365-, Brain-specific GTP-binding protein, GTP-binding protein 3, GBP-3, hGBP3, Guanine nucleotide-binding protein 3, Spastic paraplegia 3 protein A, ATL1, GBP3, SPG3A |
| Target/Specificity | This ATL1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 477-504 amino acids from the C-terminal region of human ATL1. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ATL1 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | ATL1 (HGNC:11231) |
|---|---|
| Function | Atlastin-1 (ATL1) is a membrane-anchored GTPase that mediates the GTP-dependent fusion of endoplasmic reticulum (ER) membranes, maintaining the continuous ER network. It facilitates the formation of three-way junctions where ER tubules intersect (PubMed:14506257, PubMed:18270207, PubMed:19665976, PubMed:27619977, PubMed:34817557, PubMed:38509071). Two atlastin-1 on neighboring ER tubules bind GTP and form loose homodimers through the GB1/RHD3-type G domains and 3HB regions. Upon GTP hydrolysis, the 3HB regions tighten, pulling the membranes together to drive their fusion. After fusion, the homodimer disassembles upon release of inorganic phosphate (Pi). Subsequently, GDP dissociates, resetting the monomers to a conformation ready for a new fusion cycle (PubMed:14506257, PubMed:21220294, PubMed:21368113, PubMed:23334294, PubMed:38509071). May also regulate more or less directly Golgi biogenesis (PubMed:17321752). Indirectly regulates axonal development (By similarity). |
| Cellular Location | Endoplasmic reticulum membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein. Cell projection, axon {ECO:0000250|UniProtKB:Q6PST4}. Note=Localizes to endoplasmic reticulum tubular network (PubMed:27619977). |
| Tissue Location | Expressed predominantly in the adult and fetal central nervous system. Measurable expression in all tissues examined, although expression in adult brain is at least 50-fold higher than in other tissues. Detected predominantly in pyramidal neurons in the cerebral cortex and the hippocampus of the brain. Expressed in upper and lower motor neurons (at protein level) |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The protein encoded by this gene is a GTPase and a Golgi body transmembrane protein. The encoded protein can form a homotetramer and has been shown to interact with spastin and with mitogen-activated protein kinase kinase kinase kinase 4. This protein may be involved in axonal maintenance as evidenced by the fact that defects in this gene are a cause of spastic paraplegia type 3. Three transcript variants encoding two different isoforms have been found for this gene.
REFERENCES
Cirulli, E.T., et al. Eur. J. Hum. Genet. 18(7):815-820(2010)
Park, S.H., et al. J. Clin. Invest. 120(4):1097-1110(2010)
Yoshida, T., et al. Int. J. Mol. Med. 25(4):649-656(2010)
de Leva, M.F., et al. J. Neurol. 257(3):328-331(2010)
Oguri, M., et al. Am. J. Hypertens. 23(1):70-77(2010)
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