| 產(chǎn)品編號(hào) | bs-12256R |
| 英文名稱 | phospho-CXCR4 (Ser339) Rabbit pAb |
| 中文名稱 | 磷酸化細(xì)胞表面趨化因子受體4抗體 |
| 別 名 | p-CXCR4(phospho S339); p-CD184(phospho S339); C-X-C chemokine receptor type 4; CXC-R4; CXCR-4; Stromal cell-derived factor 1 receptor; SDF-1 receptor; Fusin; Leukocyte-derived seven transmembrane domain receptor; LESTR; CD184 antigen; CXCR4_HUMAN. |
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Specific References (1) | bs-12256R has been referenced in 1 publications.
[IF=1.149] Fenlong Xue. et al. Construction and a preliminary study of paracrine effect of bone marrow-derived endothelial progenitor cell sheet. 2021 May 30 WB ; Rat.
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| 產(chǎn)品類型 | 磷酸化抗體 |
| 研究領(lǐng)域 | 腫瘤 細(xì)胞生物 免疫學(xué) 神經(jīng)生物學(xué) 干細(xì)胞 生長(zhǎng)因子和激素 新陳代謝 |
| 抗體來(lái)源 | Rabbit |
| 克隆類型 | Polyclonal |
| 克 隆 號(hào) | |
| 交叉反應(yīng) | Mouse (predicted: Human,Rat,Rabbit,Cow,Dog,Horse) |
| 產(chǎn)品應(yīng)用 | WB=1:500-2000,Flow-Cyt=1μg/Test
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 40 kDa |
| 檢測(cè)分子量 | |
| 細(xì)胞定位 | 細(xì)胞膜 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human CXCR4 around the phosphorylation site of Ser339: HS(p-S)VS |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
This gene encodes a CXC chemokine receptor specific for stromal cell-derived factor-1. The protein has 7 transmembrane regions and is located on the cell surface. It acts with the CD4 protein to support HIV entry into cells and is also highly expressed in breast cancer cells. Mutations in this gene have been associated with WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome. Alternate transcriptional splice variants, encoding different isoforms, have been characterized. Monomer. Can form dimers. Function: Receptor for the C-X-C chemokine CXCL12/SDF-1 that transduces a signal by increasing intracellular calcium ions levels and enhancing MAPK1/MAPK3 activation. Acts as a receptor for extracellular ubiquitin; leading to enhance intracellular calcium ions and reduce cellular cAMP levels. Involved in haematopoiesis and in cardiac ventricular septum formation. Plays also an essential role in vascularization of the gastrointestinal tract, probably by regulating vascular branching and/or remodeling processes in endothelial cells. Could be involved in cerebellar development. In the CNS, could mediate hippocampal-neuron survival. Acts as a coreceptor (CD4 being the primary receptor) for HIV-1 X4 isolates and as a primary receptor for some HIV-2 isolates. Promotes Env-mediated fusion of the virus. Subunit: Monomer. Can form dimmers. Subcellular Location: Cell membrane; Multi-pass membrane protein. Tissue Specificity: Expressed in numerous tissues, such as peripheral blood leukocytes, spleen, thymus, spinal cord, heart, placenta, lung, liver, skeletal muscle, kidney, pancreas, cerebellum, cerebral cortex and medulla (in microglia as well as in astrocytes), brain microvascular, coronary artery and umbilical cord endothelial cells. Isoform 1 is predominant in all tissues tested. Post-translational modifications: Phosphorylated on agonist stimulation. Rapidly phosphorylated on serine and threonine residues in the C-terminal. Phosphorylation at Ser-324 and Ser-325 leads to recruitment of ITCH, ubiquitination and protein degradation. Ubiquitinated by ITCH at the cell membrane on agonist stimulation. The ubiquitin-dependent mechanism, endosomal sorting complex required for transport (ESCRT), then targets CXCR4 for lysosomal degradation. This process is dependent also on prior Ser-/Thr-phosphorylation in the C-terminal of CXCR4. Also binding of ARRB1 to STAM negatively regulates CXCR4 sorting to lysosomes though modulating ubiquitination of SFR5S. Sulfation on Tyr-21 is required for efficient binding of CXCL12/SDF-1alpha and promotes its dimerization. O- and N-glycosylated. Asn-11 is the principal site of N-glycosylation. There appears to be very little or no glycosylation on Asn-176. N-glycosylation masks coreceptor function in both X4 and R5 laboratory-adapted and primary HIV-1 strains through inhibiting interaction with their Env glycoproteins. The O-glycosylation chondroitin sulfate attachment does not affect interaction with CXCL12/SDF-1alpha nor its coreceptor activity. DISEASE: Defects in CXCR4 are a cause of WHIM syndrome (WHIM) [MIM:193670]; also known as warts, hypogammaglobulinemia, infections and myelokathexis. WHIM syndrome is an immunodeficiency disease characterized by neutropenia, hypogammaglobulinemia and extensive human papillomavirus (HPV) infection. Despite the peripheral neutropenia, bone marrow aspirates from affected individuals contain abundant mature myeloid cells, a condition termed myelokathexis. Similarity: Belongs to the G-protein coupled receptor 1 family. SWISS: P61073 Gene ID: 7852 Database links: Entrez Gene: 7852 Human Entrez Gene: 12767 Mouse Omim: 162643 Human SwissProt: P61073 Human SwissProt: P70658 Mouse Unigene: 593413 Human |
| 產(chǎn)品圖片 |
Sample:
Lane 1: Lung (Mouse) Lysate at 40 ug
Lane 2: Spleen (Mouse) Lysate at 40 ug
Lane 3: Uterus (Mouse) Lysate at 40 ug
Lane 4: Lymph node (Mouse) Lysate at 40 ug
Primary:
Anti-phospho-CXCR4 (Ser339) (bs-12256R) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 45 kD
Observed band size: 50 kD
Blank control(mouse):Mouse Spleen Cells (fixed with 2% paraformaldehyde for 10 min at 37℃). Primary Antibody:Rabbit Anti-phospho-CXCR4 (Ser339) antibody (bs-12256R,Green); Dilution: 1μg in 100 μL 1X PBS containing 0.5% BSA; Isotype Control Antibody: Rabbit IgG(orange) ,used under the same conditions; Secondary Antibody: Goat anti-rabbit IgG-FITC(white blue), Dilution: 1:200 in 1 X PBS containing 0.5% BSA.
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