FITC标记的磷酸化转录中介因子Tif1β抗体上海沪震实业有限公司

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产品名称: FITC标记的磷酸化转录中介因子Tif1β抗体
英文名称: Anti-Phospho-TIF1 beta(Ser824)/FITC
抗体货号: HZ-3423R-FITC
产品规格: 100ul
级    别: 分析纯, , 分析纯,
产品产地: 中国/上海
品牌商标: HZbscience
价    格: 2980元
抗原: Rabbit
抗原来源: Rabbit
抗体来源: Rabbit
适用物种: 
FITCconjugate:FITC
应用范围: IF=1:50-200
更新时间: 2018/9/7 15:41:00
详细资料:  实验方法技术资料
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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

 Rabbit Anti-Phospho-TIF1 beta(Ser824)/FITC Conjugated antibody

FITC标记的***酸化转录中介因子Tif1β抗体

 

英文名称 Anti-Phospho-TIF1 beta(Ser824)/FITC
中文名称 FITC标记的***酸化转录中介因子Tif1β抗体
别    名 TIF1 beta(Phospho-Ser824); P-TIF1 beta(Ser824); KAP1 (phospho S824); p-KAP1 (phospho S824); TRIM28; TIF1 beta; E3 SUMO protein ligase TRIM28; E3 SUMO-protein ligase TRIM28; FLJ29029; KAP1; KAP 1; KAP-1; KRAB associated protein 1; KRAB interacting protein 1; KRAB-associated protein 1; KRAB-interacting protein 1; KRIP 1; KRIP-1; KRIP1; Nuclear corepressor KAP 1; Nuclear corepressor KAP-1; RING finger protein 96; RNF96; TF1B; TIF1 beta; TIF1-beta; TIF1B; TIF1B_HUMAN; Transcription intermediary factor 1 beta; Transcription intermediary factor 1-beta; TRIM28; Tripartite motif containing 28; tripartite motif containing protein 28; Tripartite motif-containing protein 28.  
规格价格 100ul/2980元 购买        大包装/询价
说 明 书 100ul  
产品类型 ***酸化抗体 
研究领域 肿瘤  细胞生物  免疫学  信号转导  转录调节因子  表观遗传学  
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat, 
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 88kDa
性    状 Lyophilized or Liquid
浓    度 1mg/ml
免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human TIF1 beta around the phosphorylation site of Ser824
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:
The KRAB (Kruppel Associated Box) domain is minimally about 45 amino acids in length and is a transcriptional repression domain found in numerous transcription factors. Over 220 KRAB zinc finger protein (KRAB ZFP) genes have been identified in the human genome. These proteins functionally repress transcription via specific interactions with KAP1 (KRAB Associated Protein 1). KAP1 is an 835 amino acid polypeptide that contains a RING finger, B boxes, and a PHD finger. KAP1 has been shown to form complexes with KRAB domain transcription factors and increase the efficiency with which they mediate repression. KAP1 has also been shown to directly interact with HP1 (heterochromatin protein 1) and KRAZ1 (Kruppel associated box containing zinc finger protein 1). KAP1 directly targets KRAZ1 to the foci of centromeric heterochromatin containing HP1alpha, helping to regulate transcriptional repression. Recent studies have shown that KAP1 mutants with the ability to bind KRAB but unable to bind HP1 leads to random distribution of KRAZ1 and strong transcriptional activation.

Function:
Nuclear corepressor for KRAB domain-containing zinc finger proteins (KRAB-ZFPs). Mediates gene silencing by recruiting CHD3, a subunit of the nucleosome remodeling and deacetylation (NuRD) complex, and SETDB1 (which specifically methylates histone H3 at 'Lys-9' (H3K9me)) to the promoter regions of KRAB target genes. Enhances transcriptional repression by coordinating the increase in H3K9me, the decrease in histone H3 'Lys-9 and 'Lys-14' acetylation (H3K9ac and H3K14ac, respectively) and the disposition of HP1 proteins to silence gene expression. Recruitment of SETDB1 induces heterochromatinization. May play a role as a coactivator for CEBPB and NR3C1 in the transcriptional activation of ORM1. Also corepressor for ERBB4. Inhibits E2F1 activity by stimulating E2F1-HDAC1 complex formation and inhibiting E2F1 acetylation. May serve as a partial backup to prevent E2F1-mediated apoptosis in the absence of RB1. Important regulator of CDKN1A/p21(CIP1). Has E3 SUMO-protein ligase activity toward itself via its PHD-type zinc finger.

Subunit:
Oligomer; the RBCC domain homotrimerizes and interacts with one molecule of KRAB to form the KRAB-KAP1 corepressor complex. Binding to a KRAB domain is an absolute requirement for silencing gene expression. Interacts with CEBPB and NR3C1 (By similarity). Interacts with a number of KRAB-ZFP proteins including ZNF10, ZFP53, ZFP68, ZNF382 and ZNF256. Interacts with NCOR1, NR3C1 and CHD3. Interacts with CEBPB (via the RING-type and PHD-type zinc fingers). Component of a ternary complex that includes TRIM28, a HP1 protein (CBX1, CBX3 OR CBX5), a KRAB domain-containing protein, and DNA. Interacts with CBX5 (via the PxVxL motif); the interaction occurs in interphase nuclei and competes for binding POGZ. Interacts with POGZ; the interaction competes for interaction with CBX5. Interacts with SETDB1; the interaction is enhanced by KAP1 sumoylation, stimulates SETB1 histone methyltransferase activity and gene silencing. Interacts (via the PHD-type zinc finger) with UBE2I; the interaction is required for sumoylation and repressor activity. Component of the TRIM28/KAP1-ERBB4-MDM2 complex involved in connecting growth factor and DNA damage responses. Interacts directly with ERBB4; the interaction represses ERBB4-mediated transcription activity. Interacts with MDM2; the interaction contributes to p53/TP53 inactivation. Component of the TRIM28/KAP1-MDM2-p53/TP53; involved in regulating p53/TP53 stabilization and activity. Interacts (via the leucine zipper alpha helical coiled-coil) with E2F1 (central region); the interaction inhibits E2F1 acetylation and transcriptional activity. Interacts with PPP1CA; the interaction dephosphorylates TRIM28 at Ser-824 and forms a complex at the p21 promoter site. Interacts with PPP1CB; the interaction is weak but is increased on dephophorylation at Ser-824. Interacts with FES/FPS. Interacts with SMARCAD1. Interacts with, and sumoylates IRF7. 

Subcellular Location:
Nucleus.

Tissue Specificity:
Expressed in all tissues tested including spleen, thymus, prostate, testis, ovary, small intestine, colon and peripheral blood leukocytes.

Post-translational modifications:
Phosphorylated upon DNA damage, probably by ATM or ATR. ATM-induced phosphorylation on Ser-824 represses sumoylation leading to the de-repression of expression of a subset of genes involved in cell cycle control and apoptosis in response to genotoxic stress. Dephosphorylation by the phosphatases, PPP1CA and PP1CB forms, allows sumoylation and expression of TRIM28 target genes. 
Sumoylation/desumoylation events regulate TRIM28-mediated transcriptional repression. Sumoylation is required for interaction with CHD3 and SETDB1 and the corepressor activity. Represses and is repressed by Ser-824 phosphorylation. Enhances the TRIM28 corepressor activity, inhibiting transcriptional activity of a number of genes including GADD45A and CDKN1A/p21. Lys-554, Lys-779 and Lys-804 are the major sites of sumoylation. In response to Dox-induced DNA damage, enhanced phosphorylation on Ser-824 prevents sumoylation and allows de-repression of CDKN1A/p21.

Similarity:
Belongs to the TRIM/RBCC family.
Contains 2 B box-type zinc fingers.
Contains 1 bromo domain.
Contains 1 PHD-type zinc finger.
Contains 1 RING-type zinc finger.

Database links:

Entrez Gene: 10155 Human

Entrez Gene: 21849 Mouse

Entrez Gene: 116698 Rat

Omim: 601742 Human

SwissProt: Q13263 Human

SwissProt: Q62318 Mouse

SwissProt: O08629 Rat

Unigene: 467408 Human

Unigene: 15701 Mouse

Unigene: 398345 Mouse

Unigene: 198494 Rat



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

KrAB(KrpPEL相关盒)结构域的长度约为45个氨基酸,是许多转录因子中发现的转录抑制域。在人类基因组中已经鉴定出超过220 krAb锌指蛋白(KrAb ZFP)基因。这些蛋白通过与KAP1(KrAb相关蛋白1)的特异性相互作用抑制转录。KAP1是一种含有835个氨基酸的多肽,包含无名指、B盒和PHD指。KAP1已被证明与KrAb结构域转录因子形成复合物,并提高其介导的阻遏的效率。KAP1也被证明直接与HP1(异染色质蛋白1)和KRAS1(含锌指蛋白1的KrpPEL关联盒)相互作用。KAP1直接将KRAZ1靶向HP1-α着丝粒异染色质的焦点,有助于调节转录抑制。最近的研究表明KAP1突变体具有结合KrAb但不能结合HP1的能力导致KRAS1的随机分布和强转录激活。

生物在线声明:以上所展示的信息由企业自行提供,内容的真实性、准确性和合法性由发布企业负责。生物在线对此不承担任何保证责任。

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