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    CREB-1 Mouse mAb (bsm-33196M)  
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    50ul/1180.00元
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    200ug(PBS only)/5600.00元
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    產(chǎn)品編號 bsm-33196M
    英文名稱(chēng) CREB-1 Mouse mAb
    中文名稱(chēng) 環(huán)腺苷酸應答元件結合蛋白單克隆抗體
    別    名 Active transcription factor CREB; cAMP response element binding protein; cAMP responsive element binding protein 1; CREB 1; CREB1; MGC9284; Transactivator protein; CREB.  
    Specific References  (1)     |     bsm-33196M has been referenced in 1 publications.
    [IF=3.414] Tang Q et al. Aqueous?extract?from?You-Gui-Yin?ameliorates?cognitive?impairment?of?chronic?renal?failure?micethrough?targeting?hippocampal?CaMKIIα/CREB/BDNF?and?EPO/EPOR pathways. J Ethnopharmacol. 2019 Jul 15;239:111925.  WB ;  Mouse.  
    研究領(lǐng)域 信號轉導  
    抗體來(lái)源 Mouse
    克隆類(lèi)型 Monoclonal
    克 隆 號 6B4
    交叉反應 Human,Mouse
    產(chǎn)品應用 WB=1:500-1000,IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500
    not yet tested in other applications.
    optimal dilutions/concentrations should be determined by the end user.
    理論分子量 37 kDa
    檢測分子量
    細胞定位 細胞核 
    性    狀 Liquid
    濃    度 1mg/ml
    免 疫 原 Recombinant human CREB-1 
    亞    型 IgG
    純化方法 affinity purified by Protein G
    緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
    保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
    注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
    PubMed PubMed
    產(chǎn)品介紹 Cyclic AMP Response Element Binding protein (CREB) is a basic / leucine zipper transcription factor that binds the cyclic AMP response element (CRE) and activates transcription in response to a variety of extracellular signals including neurotransmitters, hormones, membrane depolarization, and growth and neurotrophic factors. Activation of CREB is dependent upon the phosphorylation of serine 133. Phosphorylation occurs via p44 / 42 MAP kinase and p90RSK and also via p38 MAP kinase and MSK 1. Although CREB will bind DNA independent of its phosphorylation state, only the phosphorylated form is competent as a transcription factor. CREB binding protein (CBP), a transcriptional coactivator that directly interacts with CREB, binds to CREB in the region of serine 133. CREB appears to play an important role in learning and memory. CREB knock out mice show diminished learning ability.

    Function:
    Phosphorylation-dependent transcription factor that stimulates transcription upon binding to the DNA cAMP response element (CRE), a sequence present in many viral and cellular promoters. Transcription activation is enhanced by the TORC coactivators which act independently of Ser-133 phosphorylation. Involved in different cellular processes including the synchronization of circadian rhythmicity and the differentiation of adipose cells.

    Subunit:
    Interacts with PPRC1. Binds DNA as a dimer. This dimer is stabilized by magnesium ions. Interacts, through the bZIP domain, with the coactivators TORC1/CRTC1, TORC2/CRTC2 and TORC3/CRTC3. When phosphorylated on Ser-133, binds CREBBP (By similarity). Interacts with CREBL2; regulates CREB1 phosphorylation, stability and transcriptional activity (By similarity). Interacts (phosphorylated form) with TOX3. Interacts with ARRB1. Binds to HIPK2. Interacts with SGK1.

    Subcellular Location:
    Nucleus.

    Post-translational modifications:
    Stimulated by phosphorylation. Phosphorylation of both Ser-133 and Ser-142 in the SCN regulates the activity of CREB and participates in circadian rhythm generation. Phosphorylation of Ser-133 allows CREBBP binding (By similarity). CREBL2 positively regulates phosphorylation at Ser-133 thereby stimulating CREB1 transcriptional activity (By similarity). Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylated upon calcium influx by CaMK4 and CaMK2 on Ser-133. CaMK4 is much more potent than CaMK2 in activating CREB. Phosphorylated by CaMK2 on Ser-142. Phosphorylation of Ser-142 blocks CREB-mediated transcription even when Ser-133 is phosphorylated. Phosphorylated by CaMK1 (By similarity). Phosphorylation of Ser-271 by HIPK2 in response to genotoxic stress promotes CREB1 activity, facilitating the recruitment of the coactivator CBP. Phosphorylated at Ser-133 by RPS6KA3, RPS6KA4 and RPS6KA5 in response to mitogenic or stress stimuli.
    Sumoylated with SUMO1. Sumoylation on Lys-304, but not on Lys-285, is required for nuclear localization of this protein. Sumoylation is enhanced under hypoxia, promoting nuclear localization and stabilization.

    DISEASE:
    Defects in CREB1 may be a cause of angiomatoid fibrous histiocytoma (AFH) [MIM:612160]. A distinct variant of malignant fibrous histiocytoma that typically occurs in children and adolescents and is manifest by nodular subcutaneous growth. Characteristic microscopic features include lobulated sheets of histiocyte-like cells intimately associated with areas of hemorrhage and cystic pseudovascular spaces, as well as a striking cuffing of inflammatory cells, mimicking a lymph node metastasis. Note=A chromosomal aberration involving CREB1 is found in a patient with angiomatoid fibrous histiocytoma. Translocation t(2;22)(q33;q12) with CREB1 generates a EWSR1/CREB1 fusion gene that is most common genetic abnormality in this tumor type.
    Note=A CREB1 mutation has been found in a patient with multiple congenital anomalies consisting of agenesis of the corpus callosum, cerebellar hypoplasia, severe neonatal respiratory distress refractory to surfactant, thymus hypoplasia, and thyroid follicular hypoplasia (PubMed:22267179).

    Similarity:
    Belongs to the bZIP family.
    Contains 1 bZIP domain.
    Contains 1 KID (kinase-inducible) domain.

    SWISS:
    P16220

    Gene ID:
    1385

    Database links:

    Entrez Gene: 281713 Cow

    Entrez Gene: 1385 Human

    Entrez Gene: 12912 Mouse

    Entrez Gene: 81646 Rat

    Omim: 123810 Human

    SwissProt: P27925 Cow

    SwissProt: P16220 Human

    SwissProt: Q01147 Mouse

    SwissProt: P15337 Rat

    Unigene: 516646 Human

    Unigene: 453295 Mouse

    Unigene: 90061 Rat



    環(huán)腺苷酸應答元件結合蛋白(cAMP responsive element binding protein, CREB)是真核細胞轉錄因子,屬于A(yíng)TF/CREB家族。參與由cAMP或某些病毒蛋白質(zhì)所誘導基因轉錄的調節。
    產(chǎn)品圖片
    Sample:NIH/3T3 Cell (Mouse) Lysate at 40 ug Primary: Anti-CREB-1 (bsm-33196M) at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Mouse IgG at 1/20000 dilution Predicted band size: 37 kD Observed band size: 45 kD
    Sample: Jurkat(Human) Cell Lysate at 30 ug Huvec(Human) Cell Lysate at 30 ug U2os(Human) Cell Lysate at 30 ug Primary: Anti-CREB-1 (bsm-33196M) at 1/1000 dilution Secondary: IRDye800CW Goat Anti- Mouse IgG at 1/20000 dilution Predicted band size: 45 kD Observed band size: 43 kD
    Paraformaldehyde-fixed, paraffin embedded (mouse brain tissue); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (CREB-1) Monoclonal Antibody, Unconjugated (ascites of bsm-33196M) at 1:2000 overnight at 4°C, followed by a conjugated secondary (sp-0024) for 20 minutes and DAB staining.
    Paraformaldehyde-fixed, paraffin embedded (Mouse brain); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (CREB-1) Monoclonal Antibody, Unconjugated (ascites of bsm-33196M 6B4) at 1:2000 overnight at 4°C, followed by operating according to SP Kit(Mouse) (sp-0024) instructions and DAB staining.
    Paraformaldehyde-fixed, paraffin embedded (mouse embryos tissue); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (CREB-1) Monoclonal Antibody, Unconjugated (ascites of bsm-33196M) at 1:2000 overnight at 4°C, followed by a conjugated secondary (sp-0024) for 20 minutes and DAB staining.
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