Anti-PAX4/FITC Conjugated抗体上海钰博生物科技有限公司

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产品名称: Anti-PAX4/FITC Conjugated抗体
英文名称: Anti-PAX4/FITC
抗体货号: YB--6712R-FITC
产品规格: 20ul/50ul/100ul/200ul
级    别: , 分析纯, 见说明书
产品产地: 中国/美国
品牌商标: Ybscience
价    格: 2980元
抗原: KLH conjugated synthetic peptide derived from human PAX4
抗原来源: Rabbit
抗体来源: Rabbit
适用物种: Human, Mouse, Rat, Pig, Cow, Rabbit,
见说明书conjugate:见说明书
Isotype:见说明书
应用范围: 科研使用
更新时间: 2019/5/31 15:46:00
详细资料:  实验方法技术资料
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诚信指数:1658点
了解更多:进入公司展台
使用范围:仅限科研使用,不能应用于临床
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产品详细描述

 Anti-PAX4/FITC Conjugated抗体

产品编号 YB-6712R-FITC
英文名称 Anti-PAX4/FITC
中文名称 FITC标记的配对盒同源基因4抗体
别    名 KPD; MODY9; Paired box 4; Paired box gene 4; paired box homeotic gene 4; Paired box protein Pax-4; Paired domain gene 4; Pax4; PAX4_HUMAN.  
规格价格 100ul/2980元 购买        大包装/询价
说 明 书 100ul  
研究领域  
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat, Pig, Cow, Rabbit, 
产品应用 IF=1:50-200  
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 39kDa
性    状 Lyophilized or Liquid
浓    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human PAX4
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.
产品介绍 background:
Plays an important role in the differentiation and development of pancreatic islet beta cells. Transcriptional repressor that binds to a common element in the glucagon, insulin and somatostatin promoters. Competes with PAX6 for this same promoter binding site. Isoform 2 appears to be a dominant negative form antagonizing PAX4 transcriptional activity.
Involvement in disease; Defects in PAX4 are a cause of noninsulin-dependent diabetes mellitus (NIDDM) ; also known as diabetes mellitus type 2 or maturity-onset diabetes. NIDDM is characterized by an autosomal dominant mode of inheritance, onset during adulthood and insulin resistance.
Genetic variations in PAX4 are associated with susceptibility to insulin-dependent diabetes mellitus (IDDM). IDDM normally starts in childhood or adolescence and is caused by the body's own immune system which destroys the insulin-producing beta cells in the pancreas. Classical features are polydipsia, polyphagia and polyuria, due to hyperglycemia-induced osmotic diuresis.
Defects in PAX4 are a cause of susceptibility to diabetes mellitus ketosis-prone (KPD). KPD is an atypical form of diabetes mellitus characterized by an acute initial presentation with severe hyperglycemia and ketosis, as seen in classic type 1 diabetes, but after initiation of insulin therapy, prolonged remission is often possible with cessation of insulin therapy and maintenance of appropriate metabolic control. Metabolic studies show a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Variable levels of insulin resistance are observed, especially in obese patients. Pancreatic beta-cell autoimmunity is a rare finding.

Function:
Plays an important role in the differentiation and development of pancreatic islet beta cells. Transcriptional repressor that binds to a common element in the glucagon, insulin and somatostatin promoters. Competes with PAX6 for this same promoter binding site. Isoform 2 appears to be a dominant negative form antagonizing PAX4 transcriptional activity.

Subcellular Location:
Nucleus.

DISEASE:
Defects in PAX4 are a cause of noninsulin-dependent diabetes mellitus (NIDDM) [MIM:125853]; also known as diabetes mellitus type 2 or maturity-onset diabetes. NIDDM is characterized by an autosomal dominant mode of inheritance, onset during adulthood and insulin resistance.
Genetic variations in PAX4 are associated with susceptibility to insulin-dependent diabetes mellitus (IDDM) [MIM:222100]. IDDM normally starts in childhood or adolescence and is caused by the body's own immune system which destroys the insulin-producing beta cells in the pancreas. Classical features are polydipsia, polyphagia and polyuria, due to hyperglycemia-induced osmotic diuresis.
Defects in PAX4 are a cause of susceptibility to diabetes mellitus ketosis-prone (KPD) [MIM:612227]. KPD is an atypical form of diabetes mellitus characterized by an acute initial presentation with severe hyperglycemia and ketosis, as seen in classic type 1 diabetes, but after initiation of insulin therapy, prolonged remission is often possible with cessation of insulin therapy and maintenance of appropriate metabolic control. Metabolic studies show a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Variable levels of insulin resistance are observed, especially in obese patients. Pancreatic beta-cell autoimmunity is a rare finding.

Similarity:
Belongs to the paired homeobox family.
Contains 1 homeobox DNA-binding domain.
Contains 1 paired domain. 

Database links:
 

UniProtKB/Swiss-Prot: O43316.1



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

 

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