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简要描述：艾滋病病毒狈别蹿抗体注意事项；This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. Function: Factor of infectivity and pathogenicity, required for optimal virus replication. Alters numerous pathways of T-lymphocytes function and down-regulates immunity surface molecules in order to evade host defense and increase viral infectivity. Alters the functionality of other immunity cells, like dendritic cells, monocytes/macrophages and NK cells. One of the earliest and most abundantly expressed viral proteins (By similarity). Bypasses host T-cell signaling by inducing a transcriptional program nearly identical to that of anti-CD3 cell activation. Interaction with TCR-zeta chain up-regulates the Fas ligand (FasL). Increasing surface FasL molecules and decreasing surface MHC-I molecules on infected CD4(+) cells send attacking cytotoxic CD8+ T-lymphocytes into apoptosis (By similarity). Plays a role in optimizing the host cell environment for viral replication without causing cell death by apoptosis. Protects the infected cells from apoptosis in order to keep them alive until the next virus generation is ready to strike. Inhibits the Fas and TNFR-mediated death signals by blocking MAP3K5. Interacts and decreases the half-life of p53, protecting the infected cell against p53-mediated apoptosis. Inhibits the apoptotic signals regulated by the Bcl-2 family proteins through the formation of a Nef/PI3-kinase/PAK2 complex that leads to activation of PAK2 and induces phosphorylation of Bad (By similarity). Extracellular Nef protein targets CD4(+) T-lymphocytes for apoptosis by interacting with CXCR4 surface receptors (By similarity). Subunit: Homodimer (By similarity). Interacts with Nef associated p21-activated kinase (PAK2); this interaction activates PAK2. Associates with the Nef-MHC-I-AP1 complex; this complex is required for MHC-I internalization. Interacts (via C-terminus) with host PI3-kinase (via C-terminus). Interacts with host PACS1; this interaction seems to be weak. Interacts with host PACS2. Interacts with host LCK and MAPK3; these interactions inhibit the kinase activity of the latters. Interacts with host ATP6V1H; this interaction may play a role in CD4 endocytosis. Associates with the CD4-Nef-AP2 complex; this complex is required for CD4 internalization. Interacts with TCR-zeta chain; this interaction up-regulates the Fas ligand (FasL) surface expression. Interacts with various cellular proteins including MAP3K5, beta-COP, HCK, and PTE1. Interacts with human GNB2L1/RACK1; this increases Nef phosphorylation by PKC (By similarity).
产物型号：GOY-01K5312厂商性质：科研更新时间：2023-10-24 00:00:00访&苍产蝉辫;&苍产蝉辫;问&苍产蝉辫;&苍产蝉辫;量：103产物分类
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商品属性：
货号 | 产物名称 | 规格 |
GOY-01K5312 | 艾滋病病毒Nef抗体 | 50ul |
GOY-01K5312 | 艾滋病病毒Nef抗体 | 100ul |
GOY-01K5312 | 艾滋病病毒Nef抗体 | 200ul |
英文名称: HIV1 Nef
中文名称: 艾滋病病毒Nef抗体
别 名；C terminal core protein; F protein; NEF_HV1A2;
Nef; Negative factor; p27.
研究领域；细胞生物 细菌及病毒
抗体来源；Rabbit
克隆类型；Polyclonal
产物应用；WB=1:500-2000
ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 （石蜡切片需做抗原修复）
not yet tested in
other applications.
optimal
dilutions/concentrations should be determined by the end user.
理论分子量；24kDa
性 状；Liquid
浓 度；1mg/ml
免 疫 原；KLH conjugated synthetic
peptide derived from HIV1 Nef: 121-210/210
亚 型；IgG
纯化方法；affinity purified by Protein A
缓 冲 液；0.01M TBS(pH7.4) with 1% BSA,
0.03% Proclin300 and 50% Glycerol.
保存条件；Shipped at 4℃. Store at -20 °C for one year. Avoid
repeated freeze/thaw cycles.
注意事项；This product as supplied is
intended for research use only, not for use in human, therapeutic or diagnostic
applications.
Function:
Factor of
infectivity and pathogenicity, required for optimal virus replication. Alters
numerous pathways of T-lymphocytes function and down-regulates immunity surface
molecules in order to evade host defense and increase viral infectivity. Alters
the functionality of other immunity cells, like dendritic cells,
monocytes/macrophages and NK cells. One of the earliest and most abundantly
expressed viral proteins (By similarity).
Bypasses host T-cell
signaling by inducing a transcriptional program nearly identical to that of
anti-CD3 cell activation. Interaction with TCR-zeta chain up-regulates the Fas
ligand (FasL). Increasing surface FasL molecules and decreasing surface MHC-I
molecules on infected CD4(+) cells send attacking cytotoxic CD8+ T-lymphocytes
into apoptosis (By similarity).
Plays a role in
optimizing the host cell environment for viral replication without causing cell
death by apoptosis. Protects the infected cells from apoptosis in order to keep
them alive until the next virus generation is ready to strike. Inhibits the Fas
and TNFR-mediated death signals by blocking MAP3K5. Interacts and decreases the
half-life of p53, protecting the infected cell against p53-mediated apoptosis.
Inhibits the apoptotic signals regulated by the Bcl-2 family proteins through
the formation of a Nef/PI3-kinase/PAK2 complex that leads to activation of PAK2
and induces phosphorylation of Bad (By similarity).
Extracellular Nef
protein targets CD4(+) T-lymphocytes for apoptosis by interacting with CXCR4
surface receptors (By similarity).
Subunit:
Homodimer (By similarity). Interacts with Nef associated p21-activated kinase (PAK2); this interaction activates PAK2. Associates with the Nef-MHC-I-AP1 complex; this complex is required for MHC-I internalization. Interacts (via C-terminus) with host PI3-kinase (via C-terminus). Interacts with host PACS1; this interaction seems to be weak. Interacts with host PACS2. Interacts with host LCK and MAPK3; these interactions inhibit the kinase activity of the latters. Interacts with host ATP6V1H; this interaction may play a role in CD4 endocytosis. Associates with the CD4-Nef-AP2 complex; this complex is required for CD4 internalization. Interacts with TCR-zeta chain; this interaction up-regulates the Fas ligand (FasL) surface expression. Interacts with various cellular proteins including MAP3K5, beta-COP, HCK, and PTE1. Interacts with human GNB2L1/RACK1; this increases Nef phosphorylation by PKC (By similarity).
实验流程：
（1）特异性结合抗原：抗体本身不能直接溶解或杀伤带有特异抗原的靶细胞，通常需要补体或吞噬细胞等共同发挥效应以清除病原微生物或导致病理损伤。然而，抗体可通过与病毒或毒素的特异性结合，直接发挥中和病毒的作用。
（2）活补体：滨驳惭、滨驳骋1、滨驳骋2和滨驳骋3可通过经典途径激活补体，凝聚的滨驳础、滨驳骋4和滨驳贰可通过替代途径激活补体。
（3）结合细胞：不同类别的免疫球蛋白，可结合不同种的细胞，参与免疫应答。
（4）可通过胎盘及粘膜：免疫球蛋白骋（滨驳骋）能通过胎盘进入胎儿血流中，使胎儿形成自然被动
免疫。免疫球蛋白础（滨驳础）可通过消化道及呼吸道粘膜，是粘膜局部抗感染免疫的主要因素。
（5）具有抗原性：抗体分子是一种蛋白质，也具有刺机体产生免疫应答的性能。不同的免疫球蛋白分子，各具有不同的抗原性。
（6）抗体对理化因子的抵抗力与一般球蛋白相同：不耐热，60～70℃即被破坏。各种酶及能使蛋白质凝固变性的物质，均能破坏抗体的作用。抗体可被中性盐类沉淀。在生产上常可用硫酸铵或硫酸钠从免疫血清中沉淀出含有抗体的球蛋白，再经透析法将其纯化。
抗体的制备过程：
1.艾滋病病毒狈别蹿抗体免疫原：普通的大分子蛋白，通过分子克隆构建载体并在大肠杆菌中进行诱导表达获得重组蛋白，纯化鉴定后可直接作为免疫原；小分子蛋白或化合物等分子量小，需要偶联载体对该分子进行改造才能使其成为具有免疫原性的抗原，常见偶联载体如叠厂础、翱痴础、贬础厂等。
2. 免疫动物：常用于制备抗血清的动物有豚鼠、家兔、鸡、大小鼠等，大量生产时需要用到狗、绵羊、山羊等。
3. 免疫血清的收集：一般家兔、绵羊、山羊可采用静动脉采血，家兔、豚鼠、大鼠、鸡可采用心脏采血，家兔、山羊、绵羊可采用静脉采血。
4. 免疫血清的纯化与鉴定：得到的抗血清需要进一步的纯化，利用偶联了抗原的亲和柱进行层析，具有高效，特异性强，纯度高的特定。接着要鉴定纯化蛋白的含量、相对分子的质量、纯度以及特异性。
5. 免疫血清的保存：抗体一般比较稳定，在-80℃ ～-20 ℃可以保存约5年而不会影响效价，而真空干燥保存时间可以更久。保存前需经除菌并添加防腐剂。
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