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Rabbit Anti-MLF1/MLF2 /Cy3 Conjugated antibody (bs-9179R-Cy3)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-9179R-Cy3
英文名稱 Rabbit Anti-MLF1/MLF2 /Cy3 Conjugated antibody
中文名稱 Cy3標(biāo)記的髓細(xì)胞性白血病蛋白1抗體
別    名 Hls7; MLF1; MLF2; MLF3; MLF1_HUMAN; Myelodysplasia myeloid leukemia factor 1; Myelodysplasia-myeloid leukemia factor 1; Myeloid leukemia factor 1; myeloid leukemia factor 1 variant 1; myeloid leukemia factor 1 variant 2; myeloid leukemia factor 1 variant 3.  
規(guī)格價(jià)格 100ul/2980元 購買        大包裝/詢價(jià)
說 明 書 100ul  
研究領(lǐng)域 腫瘤  心血管  細(xì)胞生物  免疫學(xué)  染色質(zhì)和核信號(hào)  信號(hào)轉(zhuǎn)導(dǎo)  干細(xì)胞  細(xì)胞周期蛋白  細(xì)胞分化  細(xì)胞類型標(biāo)志物  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Pig, Cow, Sheep, )
產(chǎn)品應(yīng)用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 31kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human MLF1/2/3
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 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(chǎn)品介紹 background:
Involved in lineage commitment of primary hemopoietic progenitors by restricting erythroid formation and enhancing myeloid formation. Interferes with erythropoietin-induced erythroid terminal differentiation by preventing cells from exiting the cell cycle through suppression of CDKN1B/p27Kip1 levels. Suppresses RFWD2/COP1 activity via CSN3 which activates p53 and induces cell cycle arrest. Binds DNA and affects the expression of a number of genes so may function as a transcription factor in the nucleus.

Function:
Involved in lineage commitment of primary hemopoietic progenitors by restricting erythroid formation and enhancing myeloid formation. Interferes with erythropoietin-induced erythroid terminal differentiation by preventing cells from exiting the cell cycle through suppression of CDKN1B/p27Kip1 levels. Suppresses RFWD2/COP1 activity via CSN3 which activates p53 and induces cell cycle arrest. Binds DNA and affects the expression of a number of genes so may function as a transcription factor in the nucleus.

Subunit:
Interacts with MLF1IP. Also interacts with NRBP1/MADM, YWHAZ/14-3-3-zeta and HNRPUL2/MANP. NRBP1 recruits a serine kinase which phosphorylates both itself and MLF1. Phosphorylated MLF1 then binds to YWHAZ and is retained in the cytoplasm. Retained in the nucleus by binding to HNRPUL2. Binds to COPS3/CSN3 which is required for suppression of RFWD2 and activation of p53.

Subcellular Location:
Cytoplasm. Nucleus. In non-hematopoietic cells, resides primarily in the cytoplasm with some punctate nuclear localization. Shuttles between the cytoplasm and nucleus. In hematopoietic cells, located preferentially in the nucleus. Found in the nucleolus when fused to NPM.

Tissue Specificity:
Most abundant in testis, ovary, skeletal muscle, heart, kidney and colon. Low expression in spleen, thymus and peripheral blood leukocytes.

Post-translational modifications:
Phosphorylation is required for binding to YWHAZ (By similarity).

DISEASE:
Note=A chromosomal aberration involving MLF1 is a cause of myelodysplastic syndrome (MDS). Translocation t(3;5)(q25.1;q34) with NPM1/NPM.

Similarity:
Belongs to the MLF family.

Database links:

Entrez Gene: 79682 Human

Entrez Gene: 71876 Mouse

Entrez Gene: 306464 Rat

Omim: 611511 Human

SwissProt: Q2KIW5 Cow

SwissProt: Q71F23 Human

SwissProt: Q8C4M7 Mouse

SwissProt: Q4V8G7 Rat

Unigene: 575032 Human

Unigene: 217385 Mouse

Unigene: 22108 Mouse

Unigene: 128609 Rat



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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