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。
TLR4 Rabbit pAb
- 产品详情
- 实验流程
Application 
| WB, IHC-P, IHC-F, IF |
|---|---|
| Primary Accession | Q9QX05 |
| Other Accession | Q9QX05 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 96072 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from rat TLR4 |
| Epitope Specificity | 751-835/835 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SIMILARITY | Belongs to the Toll-like receptor family. Contains 18 LRR (leucine-rich) repeats. Contains 1 LRRCT domain. Contains 1 TIR domain. |
| Post-translational modifications | N-glycosylated. Glycosylation of Asn-526 and Asn-575 seems to be necessary for the expression of TLR4 on the cell surface and the LPS-response. Likewise, mutants lacking two or more of the other N-glycosylation sites were deficient in interaction with LPS. |
| DISEASE | Genetic variation in TLR4 is associated with age-related macular degeneration type 10 (ARMD10) [MIM:611488]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | The Toll-like receptor 4 by activating natural immunity, specific immune response involved in the start-up, Toll-like receptor 4 as an important signal transduction transmembrane receptor involved in the toxin-induced inflammation in the pathological process, its mechanisms of control On a growing concern. all regions were either double-stranded or sequenced with an alternatechemistry or covered by high quality data(i.e., phred quality >=30); an attempt was made to resolve all sequencing problems, such as compressions and repeats; all regions were covered by at least one subclone; and the assembly was confirmed by restriction digest, except on the rare occasion of the clone being a YAC. The following abbreviations are used to associate primary accession numbers given in the feature table with their source databases: Em:, EMBL; Sw:, SWISSPROT; Tr:, TREMBL; Wp:, WORMPEP; Information on the WORMPEP database can be found at. TLR-4 plays an important role in microvascular leakage and leukocyte adhesion under the inflammatory condition associated with nonseptic thermal injury. |
| Gene ID | 29260 |
|---|---|
| Other Names | ARMD10; CD284; TLR-4; TOLL; Lps; Ly87; Ran/M1; Rasl2-8; TLR4_HUMAN; TLR4; hToll; TLR4_MOUSE; TLR4_RAT; Toll4; toll like receptor 4; toll-like receptor 4 |
| Dilution | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500,Flow-Cyt=2ug/Test |
| 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. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | Tlr4 |
|---|---|
| Function | Transmembrane receptor that functions as a pattern recognition receptor recognizing pathogen- and damage-associated molecular patterns (PAMPs and DAMPs) to induce innate immune responses via downstream signaling pathways. At the plasma membrane, cooperates with LY96 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Also involved in LPS-independent inflammatory responses triggered by free fatty acids, such as palmitate, and Ni(2+). Mechanistically, acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Alternatively, CD14-mediated TLR4 internalization via endocytosis is associated with the initiation of a MYD88-independent signaling via the TICAM1-TBK1-IRF3 axis leading to type I interferon production. In addition to the secretion of proinflammatory cytokines, initiates the activation of NLRP3 inflammasome and formation of a positive feedback loop between autophagy and NF-kappa-B signaling cascade. In complex with TLR6, promotes inflammation in monocytes/macrophages by associating with TLR6 and the receptor CD86. Upon ligand binding, such as oxLDL or amyloid-beta 42, the TLR4:TLR6 complex is internalized and triggers inflammatory response, leading to NF-kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway. In myeloid dendritic cells, vesicular stomatitis virus glycoprotein G but not LPS promotes the activation of IRF7, leading to type I IFN production in a CD14-dependent manner. |
| Cellular Location | Cell membrane {ECO:0000250|UniProtKB:O00206}; Single-pass type I membrane protein {ECO:0000250|UniProtKB:O00206} Early endosome {ECO:0000250|UniProtKB:O00206}. Cell projection, ruffle {ECO:0000250|UniProtKB:Q9QUK6}. Note=Upon complex formation with CD36 and TLR6, internalized through dynamin-dependent endocytosis Colocalizes with RFTN1 at cell membrane and then together with RFTN1 moves to endosomes, upon lipopolysaccharide stimulation {ECO:0000250|UniProtKB:O00206} |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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