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Product Name Anti-CREB-1/AF594 Chinese Name AF594标记的环腺苷酸应答元件Binding protein抗体 Alias Active transcription factor CREB; cAMP response element binding protein; cAMP responsive element binding protein 1; CREB1; CREB 1; CREB1; MGC9284; Transactivator protein; CREB; CREB1_HUMAN. Research Area immunology Chromatin and nuclear signals Signal transduction transcriptional regulatory factor Immunogen Species Rabbit Clonality Polyclonal React Species Human, (predicted: Mouse, Rat, Chicken, Dog, Pig, Cow, Sheep, ) Applications IF=1:50-200
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.Molecular weight 37kDa Form Lyophilized or Liquid Concentration 1mg/ml immunogen KLH conjugated synthetic peptide derived from human CREB-1 Lsotype IgG Purification affinity purified by Protein A Storage Buffer 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Storage 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. Product Detail background:
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.
Database links:
Entrez Gene: 1385 Human
Entrez Gene: 12912 Mouse
Omim: 123810 Human
SwissProt: P16220 Human
SwissProt: Q01147 Mouse
Unigene: 516646 Human
Unigene: 453295 Mouse
Unigene: 90061 Rat
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
环腺苷酸应答元件Binding protein(cAMP responsive element binding protein, CREB)是真核细胞转录因子,属于ATF/CREB家族。参与由cAMP或某些病毒蛋白质所诱导基因转录的调节。
ATF/CREB家族相关蛋白
SL0517R ATF-1 活化复制因子1
SL0518R ATF-2 活化复制因子2
SL0519R ATF-3 活化复制因子3
SL0035M CREB 非磷酸化环腺苷酸应答元件Binding protein(抗体)
SL0036R P-CREB 磷酸化环腺苷酸应答元件Binding protein(抗体)
Username | Quantity | bought time |
Ja*** | 2 | 2024-03-20 |
Iv*** | 2 | 2024-03-01 |
Al*** | 1 | 2023-05-21 |
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