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- jlcR6165
- 国内
- 2025年07月08日
- WB,ELISA等
- 人/动物/植物
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- 详细信息
- 文献和实验
- 技术资料
- 供应商：
江西江蓝纯生物试剂有限公司
- 库存：
42
- 克隆性：
单克隆
- 保质期：
1年
- 抗体英文名：
GTPase HRAS
- 抗体名：
转化蛋白p21抗体（原癌基因H-ras抗体）
- 适应物种：
人/动物/植物
- 应用范围：
WB,ELISA等
- 浓度：
1mg/ml
- 保存条件：
-20 °
- 规格：
100ul/200ul
| 规格： | 100ul | 产品价格： | ¥1580.0 |
|---|---|---|---|
| 规格： | 200ul | 产品价格： | ¥2480.0 |
产品货号 : jlcR6165
英文名称 : GTPase HRAS
中文名称 : 转化蛋白p21抗体（原癌基因H-ras抗体）
别 名 : p21ras; Transforming protein p21; GTPase HRas; GTPase KRas; HRas; HRAS1; KRas; KRAS2; RASH; RASK; RASH_HUMAN; RASK_HUMAN.
研究领域 : 肿瘤 细胞生物 信号转导 转录调节因子 G蛋白偶联受体
抗体来源 : Rabbit
克隆类型 : Polyclonal
交叉反应 : Human, Mouse, Rat, Chicken, Cow, Horse,
产品应用 : WB=1:500-2000 ELISA=1:500-1000 IHC-F=1:400-800 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.
分 子 量 : 21kDa
细胞定位 : 细胞核 细胞浆
性 状 : Lyophilized or Liquid
浓 度 : 1mg/ml
免 疫 原 : KLH conjugated synthetic peptide derived from human HRAS+KRAS:51-150/189
亚 型 : IgG
纯化方法 : affinity purified by Protein A
储 存 液 : 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件 : Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. 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.
PubMed : PubMed
产品介绍background:
The KRAS gene encodes the human cellular homolog of a transforming gene isolated from the Kirsten rat sarcoma virus. The RAS proteins are GDP/GTP-binding proteins that act as intracellular signal transducers. The most well-studied members of the RAS (derived from 'RAt Sarcoma' virus) gene family include KRAS, HRAS, and NRAS. These genes encode immunologically related proteins with a molecular mass of 21 kD and are homologs of rodent sarcoma virus genes that have transforming abilities. While these wildtype cellular proteins in humans play a vital role in normal tissue signaling, including proliferation, differentiation, and senescence, mutated genes are potent oncogenes that play a role in many human cancers.
Function:
Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
Subunit:
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) (By similarity). Forms a signaling complex with RASGRP1 and DGKZ. Interacts with RASSF5. Interacts with PDE6D. Interacts with IKZF3. Interacts with GNB2L1. Interacts with PIK3CG; the interaction is required for membrane recruitment and beta-gamma G protein dimer-dependent activation of the PI3K gamma complex PIK3CG:PIK3R6 (By similarity).
Subcellular Location:
Isoform 2: Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Note=Colocalizes with GNB2L1 to the perinuclear region.
Tissue Specificity:
Widely expressed.
Post-translational modifications:
Palmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi.
S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation.
The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation.
Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs) (By similarity).
DISEASE:
Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:218040]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.
Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:218040]. CMEMS is a variant of Costello syndrome.
Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:607464]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms.
Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors.
Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences.
Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).
Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:163200]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.
Similarity:
Belongs to the small GTPase superfamily. Ras family.
SWISS:
P01112
Gene ID:
3265
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品图片 :
英文名称 : GTPase HRAS
中文名称 : 转化蛋白p21抗体（原癌基因H-ras抗体）
别 名 : p21ras; Transforming protein p21; GTPase HRas; GTPase KRas; HRas; HRAS1; KRas; KRAS2; RASH; RASK; RASH_HUMAN; RASK_HUMAN.
研究领域 : 肿瘤 细胞生物 信号转导 转录调节因子 G蛋白偶联受体
抗体来源 : Rabbit
克隆类型 : Polyclonal
交叉反应 : Human, Mouse, Rat, Chicken, Cow, Horse,
产品应用 : WB=1:500-2000 ELISA=1:500-1000 IHC-F=1:400-800 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.
分 子 量 : 21kDa
细胞定位 : 细胞核 细胞浆
性 状 : Lyophilized or Liquid
浓 度 : 1mg/ml
免 疫 原 : KLH conjugated synthetic peptide derived from human HRAS+KRAS:51-150/189
亚 型 : IgG
纯化方法 : affinity purified by Protein A
储 存 液 : 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件 : Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. 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.
PubMed : PubMed
产品介绍background:
The KRAS gene encodes the human cellular homolog of a transforming gene isolated from the Kirsten rat sarcoma virus. The RAS proteins are GDP/GTP-binding proteins that act as intracellular signal transducers. The most well-studied members of the RAS (derived from 'RAt Sarcoma' virus) gene family include KRAS, HRAS, and NRAS. These genes encode immunologically related proteins with a molecular mass of 21 kD and are homologs of rodent sarcoma virus genes that have transforming abilities. While these wildtype cellular proteins in humans play a vital role in normal tissue signaling, including proliferation, differentiation, and senescence, mutated genes are potent oncogenes that play a role in many human cancers.
Function:
Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
Subunit:
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) (By similarity). Forms a signaling complex with RASGRP1 and DGKZ. Interacts with RASSF5. Interacts with PDE6D. Interacts with IKZF3. Interacts with GNB2L1. Interacts with PIK3CG; the interaction is required for membrane recruitment and beta-gamma G protein dimer-dependent activation of the PI3K gamma complex PIK3CG:PIK3R6 (By similarity).
Subcellular Location:
Isoform 2: Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Note=Colocalizes with GNB2L1 to the perinuclear region.
Tissue Specificity:
Widely expressed.
Post-translational modifications:
Palmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi.
S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation.
The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation.
Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs) (By similarity).
DISEASE:
Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:218040]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.
Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:218040]. CMEMS is a variant of Costello syndrome.
Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:607464]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms.
Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors.
Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences.
Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).
Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:163200]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.
Similarity:
Belongs to the small GTPase superfamily. Ras family.
SWISS:
P01112
Gene ID:
3265
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品图片 :
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文献和实验相关实验
Ras 信号通路 很多生长因子如EGF、PDGF、FGF等激活受体酪氨酸激酶后，通过中介分子可活化由原癌基因FaS编码的Ras蛋白 ，后者能进一步催化其底物蛋白的酪氨酸磷酸化反应，并引发蛋白磷酸化的级联反应，最终导致细胞的增殖效应。由于Ras蛋白为多种生长因子信号转导过程所共有，故把此信号转导途径称为Ras通路。 Ras蛋白是癌基因las的编码产物，人类有3种ras基因，即H―FaS、K―las和N―Fas，分布于不同染色体上，能编码蛋白质P21。所有的Ras―P21均有结合鸟
（qualitative model）。例如在膀胱癌 细胞株 由于癌基因ras的12位密码子GGC变为GTC，使甘氨酸变为缬氨酸，结果导致细胞具有转化细胞的特征。现今已在膀胱癌、结肠癌等许多肿瘤发现了ras基因，后者编码一种膜蛋白，称为p21蛋白。 （2）易位激活：易位导致癌基因的重排或融合，产生异常的蛋白而使细胞转化。例如慢性粒细胞白血病9；22易位，形成了一种结构与功能异常的融合基因bcr-abl。它编码的蛋白能促成细胞的恶性转化。 原癌基因通过易位插到强力的启动
肝刺激因子对人肝癌细胞BEL-7402 p21ras表达的影响
［22］介绍的方法进行Ras蛋白杂交。简要为: NC膜于4℃、5%脱脂奶粉(安怡高钙脱脂奶粉, 新西兰)TBST溶液中封闭过夜; 先后与抗H-Ras单克隆抗体(1∶100, sc-35, 美国Santa Cruz公司)及辣根过氧化物酶标记抗大鼠IgG(1∶1?000, 美国Santa Cruz公司)室温下孵育各1 h。之后, 将膜充分漂洗, 迅速加入发光试剂(美国Santa Cruz公司)进行发光自显影; 曝光于X光片上的自显影信号强度经密度扫描仪(GS-700,美国Bio-Rad公司)扫描并经
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转化蛋白p21抗体（原癌基因H-ras抗体）
¥1580 - 2480
