CREB3L1 Antibody
(Synonyms: OASIS, PSEC0238, CREB3L1, Cyclic AMP-responsive element-binding protein 3-like protein 1, cAMP-responsive element-binding protein 3-like protein 1, Old astrocyte specifically-induced substance)CREB3L1 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to CREB3L1.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, FC
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Reactivity :
Human, Mouse
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Formulation:
Supplied in PBS (pH 7.4), containing 30% glycerol, and 0.01% sodium azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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FC
FC: Flow Cytometry
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|---|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:100-200 | 1:10-50 |
Product Details
CREB3L1 Antibody is a Rabbit-derived and non-conjugated IgG Polyclonal antibody, targeting to CREB3L1.
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Host Rabbit
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Clonality Polyclonal
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Species ReactivityHuman, Mouse
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Observed Molecular WeightObserved band size: 57; 48 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 57 kDa
Synthetic peptide corresponding to the C-terminal region of human CREB3L1.
Endogenous
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS (pH 7.4), containing 30% glycerol, and 0.01% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
CREB3L1 is a Precursor of the transcription factor form (Processed cyclic AMP-responsive element-binding protein 3-like protein 1), which is embedded in the endoplasmic reticulum membrane with N-terminal DNA-binding and transcription activation domains oriented toward the cytosolic face of the membrane. In response to ER stress or DNA damage, transported to the Golgi, where it is cleaved in a site-specific manner by resident proteases S1P/MBTPS1 and S2P/MBTPS2. The released N-terminal cytosolic domain is translocated to the nucleus where it activates transcription of specific target genes involved in the cell-cycle progression inhibition[1][2][3][4].
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Subcellular Localization
Endoplasmic reticulum membrane
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Expression
Tissue_Specificity: Expressed in several tissues, with highest levels in pancreas and prostate. Expressed at relatively lower levels in brain. -
Isoforms & Post-Translational Modification
CREB3L1 has 2 isoforms, Q96BA8-1: amino acid length is 519, molecular weight is 57005 Da (predicted); Q96BA8-2: amino acid length is 431, molecular weight is 47783 Da (predicted).
Upon ER stress or DNA damage, translocated to the Golgi apparatus, where it is processed by regulated intramembrane proteolysis (RIP) to release the cytosol-facing N-terminal transcription factor domain. The cleavage is performed sequentially by site-1 and site-2 proteases (S1P/MBTPS1 and S2P/MBTPS2). RIP is induced by TGFB1 and ceramide. -
Subunit
Interacts with SMAD4, the interaction takes place upon TGFB1 induction and SMAD4 acts as a CREB3L1 coactivator to induce the expression of genes involved in assembly of collagen extracellular matrix
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SwissProt ID
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Synonyms
OASIS, PSEC0238, CREB3L1, Cyclic AMP-responsive element-binding protein 3-like protein 1, cAMP-responsive element-binding protein 3-like protein 1, Old astrocyte specifically-induced substance
Documentation
[1]. Omori Y, et al. OASIS is a transcriptional activator of CREB/ATF family with a transmembrane domain. Biochem Biophys Res Commun. 2002 Apr 26;293(1):470-7. [Content Brief]
[2]. Murakami T, et al. Cleavage of the membrane-bound transcription factor OASIS in response to endoplasmic reticulum stress. J Neurochem. 2006 Feb;96(4):1090-100. [Content Brief]
[3]. Chen Q, et al. Sustained induction of collagen synthesis by TGF-β requires regulated intramembrane proteolysis of CREB3L1. PLoS One. 2014;9(10):e108528. [Content Brief]
[4]. Denard B, et al. The membrane-bound transcription factor CREB3L1 is activated in response to virus infection to inhibit proliferation of virus-infected cells. Cell Host Microbe. 2011 Jul 21;10(1):65-74. [Content Brief]