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Rabbit Anti-KMT3B/PE-Cy7 Conjugated antibody (bs-8170R-PE-Cy7)
訂購熱線:400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產品編號 bs-8170R-PE-Cy7
英文名稱 Rabbit Anti-KMT3B/PE-Cy7 Conjugated antibody
中文名稱 PE-Cy7標記的組蛋白甲基化KMT3B抗體(雄激素受體激活蛋白)
別    名 Androgen receptor coactivator 267 kDa protein; Androgen receptor-associated protein of 267 kDa; ARA267; H3 K36 HMTase; H3-K36-HMTase; H4 K20 HMTase; H4-K20-HMTase; Histone-lysine N-methyltransferase, H3 lysine-36 and H4 lysine-20 specific; KMT3B; Lysine N-methyltransferase 3B; NR binding SET domain containing protein; NR-binding SET domain-containing protein; Nsd1; NSD1_HUMAN; Nuclear receptor binding SET domain containing protein 1; Nuclear receptor-binding SET domain-containing protein 1.  
規格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 腫瘤  細胞生物  信號轉導  表觀遺傳學  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 (predicted: Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit, Sheep, )
產品應用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 296kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human KMT3B/NSD1/ARA267
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 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.
產品介紹 background:
This gene encodes a protein containing a SET domain, 2 LXXLL motifs, 3 nuclear translocation signals (NLSs), 4 plant homeodomain (PHD) finger regions, and a proline-rich region. The encoded protein enhances androgen receptor (AR) transactivation, and this enhancement can be increased further in the presence of other androgen receptor associated coregulators. This protein may act as a nucleus-localized, basic transcriptional factor and also as a bifunctional transcriptional regulator. Mutations of this gene have been associated with Sotos syndrome and Weaver syndrome. One version of childhood acute myeloid leukemia is the result of a cryptic translocation with the breakpoints occurring within nuclear receptor-binding Su-var, enhancer of zeste, and trithorax domain protein 1 on chromosome 5 and nucleoporin, 98-kd on chromosome 11. Two transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq, Jul 2008].

Function:
Histone methyltransferase. Preferentially methylates'Lys-36' of histone H3 and 'Lys-20' of histone H4 (in vitro).Transcriptional intermediary factor capable of both negatively orpositively influencing transcription, depending on the cellularcontext.

Subunit:
Interacts with the ligand-binding domains of RARA andTHRA in the absence of ligand; in the presence of ligand theinteraction is severely disrupted but some binding still occurs.Interacts with the ligand-binding domains of RXRA and ESRRA only inthe presence of ligand. Interacts with ZNF496 (By similarity).Interacts with AR DNA- and ligand-binding domains.

Subcellular Location:
Nucleus. Chromosome (Probable).

Tissue Specificity:
Expressed in the fetal/adult brain, kidney,skeletal muscle, spleen, and the thymus, and faintly in the lung.

DISEASE:
Defects in NSD1 are the cause of Sotos syndrome type 1(SOTOS1) [MIM:117550]; also known as cerebral gigantism. It is adisorder characterized by excessively rapid growth, acromegalicfeatures, and a nonprogressive cerebral disorder with mentalretardation. High-arched palate and prominent jaw are noted inseveral patients. Most cases of Sotos syndrome are sporadic and mayrepresent new dominant mutation.
Defects in NSD1 are the cause of Weaver syndrome type 1(WVS1) [MIM:277590]. A syndrome of accelerated growth and osseousmaturation, unusual craniofacial appearance, hoarse and low-pitchedcry, and hypertonia with camptodactyly. Distinguishing features ofWeaver syndrome include broad forehead and face, ocularhypertelorism, prominent wide philtrum, micrognathia, deephorizontal chin groove, and deep-set nails. In addition, carpalbone development is advanced over the rest of the hand.
Defects in NSD1 are a cause of Beckwith-Wiedemannsyndrome (BWS) [MIM:130650]. BWS is a genetically heterogeneousdisorder characterized by anterior abdominal wall defects includingexomphalos (omphalocele), pre- and postnatal overgrowth, andmacroglossia. Additional less frequent complications includespecific developmental defects and a predisposition to embryonaltumors.
Note=A chromosomal aberration involving NSD1 is found inchildhood acute myeloid leukemia. Translocation t(5;11)(q35;p15.5)with NUP98.
Note=A chromosomal aberration involving NSD1 is found inan adult form of myelodysplastic syndrome (MDS). Insertion of NUP98into NSD1 generates a NUP98-NSD1 fusion product.

Similarity:
Belongs to the histone-lysine methyltransferasefamily.
Contains 1 AWS domain.
Contains 4 PHD-type zinc fingers.
Contains 1 post-SET domain.
Contains 2 PWWP domains.
Contains 1 SET domain.

Database links:
UniProtKB/Swiss-Prot: Q96L73.1

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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