KRAS Rabbit pAb, HRP conjugated(bs-1033R-HRP)-100ul

KRAS Rabbit pAb, HRP conjugate

d(bs-1033R-HRP)-100ul
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  • ¥2980
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  • bs-1033R-HRP
  • 2025年09月30日
  • 产品信息以Bioss网站为准
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      100ul

    产品编号bs-1033R-HRP
    英文名称KRAS Rabbit pAb, HRP conjugated
    中文名称HRP标记的原癌基因K-ras抗体
    英文别名C-K-RAS; c-Ki-ras; c-Ki-ras p21; Ha-ras; K-RAS B; K-RAS2A; K-RAS2B; K-RAS4A; KI-RAS; KI-RAS4B; KRAS; KRAS1; KRAS2; MGC7141; NS; NS3; p21; p21B; p21ras; RAS; RAS1; RASH; RASK2.
    产品应用WB=1:500-2000, IHC-P=1:100-500, IHC-F=1:100-500

    Not yet tested in other applications.
    Optimal working dilutions must be determined by the end user.

    抗体来源Rabbit
    免疫原KLH conjugated synthetic peptide derived from human K-ras
    亚型IgG
    纯化方法affinity purified by Protein A
    克隆类型Polyclonal
    浓度1mg/ml
    储存液0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
    研究领域

    Cancer > Signal transduction > G protein signaling > Small G proteins > Ras family

    Epigenetics and Nuclear Signaling > Transcription > Cancer susceptibility > Proto-oncogenes

    Signal Transduction > Signaling Pathway > G Protein Signaling > Small G Proteins > Ras Family

    亚基In its GTP-bound form interacts with PLCE1. Interacts with TBC1D10C. Interacts with RGL3. Interacts with HSPD1. Found in a complex with at least BRAF, HRAS1, MAP2K1, MAPK3 and RGS14. Interacts (active GTP-bound form) with RGS14 (via RBD 1 domain). Forms a signaling complex with RASGRP1 and DGKZ. Interacts with RASSF5. Interacts with PDE6D. Interacts with IKZF3. Interacts with GNB2L1.
    亚细胞定位Cell membrane. Cell membrane; Lipid-anchor; Cytoplasmic side. Golgi apparatus. Golgi apparatus membrane; Lipid-anchor. Isoform 2: Nucleus. Cytoplasm. Cytoplasm, perinuclear region.
    组织特异性Widely expressed.
    相似性Belongs to the small GTPase superfamily. Ras family.
    功能Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
    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.
    背景资料This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region. [provided by RefSeq]Ras, a proto-oncogene, is a small G-protein that has 3 primary isoforms (H-Ras, N-Ras, and K-Ras) that differ in there approximately 20 C-terminal amino acids. H-Ras was first discovered as a transforming product the retrovirus Harvey murine virus and K-Ras of Kirten sarcoma virus. Ras is a heavily studied target of both academic and pharmaceutical research because of its implications in various pathways and diseases as well as being mutated in a large number of human cancers. Ras is most notably the activator of the Erk/MAPK kinase pathway as activator of Raf, as well as an activator of PI3 Kinase (PI3K). In its oncogenic, mutated state, Ras is unable to hydrolyze GTP to GDP, thus staying in an active state and activating numerous pathways including the MAPK pathway through its activation of Raf, but also others as well that include PI3 Kinase and RalGDS. One path that the pharmaceutical industry has taken to control Ras and its activity is by finding what some consider its Achilles’ heel. For its activation, Ras must localize to the plasma membrane, but interestingly, it lacks a transmembrane domain. To achieve this, Ras must first undergo a post-translational modification (PTM) known as prenylation or geranylation at its C-terminal CAAX motif. For this to take place, a controlled three step process must occur. The first step in the process is the prenylation or geranylation of the C in the CAAX motif that is initiated by the covalent attachment of farnesyl groups to the cysteine that is catalyzed by the . After this modification, the and heterodimer enzymes farnesyl transferases –aaX of the motif is proteolytically removed via Rce1 (Ras Converting Enzyme 1), a membrane associated endoprotease, by a mechanism that is still not fully understood. Finally, the C-terminal prenylcysteine is now methlylated by ICMT (Isoprenylcysteine Carboxymethyl Transferase). These drugs have yet to pass clinical trials though and there is doubt that they will ever be successful in treating tumors associated with Ras activation.

     

    应用推荐稀释比例
    {WB}{1:500-2000}
    {IHC-P}{1:100-500}
    {IHC-F}{1:100-500}

     

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