Mouse Stk11 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| IF, IHC-P, WB, E |
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Primary Accession | Q9WTK7 |
Other Accession | NP_035622.1 |
Reactivity | Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 49267 Da |
Antigen Region | 393-420 aa |
Gene ID | 20869 |
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Other Names | Serine/threonine-protein kinase STK11, Liver kinase B1 homolog, LKB1, mLKB1, Stk11 {ECO:0000312|MGI:MGI:1341870} |
Target/Specificity | This Mouse Stk11 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 393-420 amino acids from the C-terminal region of mouse Stk11. |
Dilution | IF~~1:25 WB~~1:500-1:1000 IHC-P~~1:25 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | Mouse Stk11 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | Stk11 {ECO:0000312|MGI:MGI:1341870} |
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Function | Tumor suppressor serine/threonine-protein kinase that controls the activity of AMP-activated protein kinase (AMPK) family members, thereby playing a role in various processes such as cell metabolism, cell polarity, apoptosis and DNA damage response. Acts by phosphorylating the T-loop of AMPK family proteins, thus promoting their activity: phosphorylates PRKAA1, PRKAA2, BRSK1, BRSK2, MARK1, MARK2, MARK3, MARK4, NUAK1, NUAK2, SIK1, SIK2, SIK3 and SNRK but not MELK. Also phosphorylates non-AMPK family proteins such as STRADA, PTEN and possibly p53/TP53. Acts as a key upstream regulator of AMPK by mediating phosphorylation and activation of AMPK catalytic subunits PRKAA1 and PRKAA2 and thereby regulates processes including: inhibition of signaling pathways that promote cell growth and proliferation when energy levels are low, glucose homeostasis in liver, activation of autophagy when cells undergo nutrient deprivation, and B-cell differentiation in the germinal center in response to DNA damage. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton. Required for cortical neuron polarization by mediating phosphorylation and activation of BRSK1 and BRSK2, leading to axon initiation and specification. Involved in DNA damage response: interacts with p53/TP53 and recruited to the CDKN1A/WAF1 promoter to participate in transcription activation. Able to phosphorylate p53/TP53; the relevance of such result in vivo is however unclear and phosphorylation may be indirect and mediated by downstream STK11/LKB1 kinase NUAK1. Also acts as a mediator of p53/TP53-dependent apoptosis via interaction with p53/TP53: translocates to the mitochondrion during apoptosis and regulates p53/TP53-dependent apoptosis pathways. Regulates UV radiation-induced DNA damage response mediated by CDKN1A. In association with NUAK1, phosphorylates CDKN1A in response to UV radiation and contributes to its degradation which is necessary for optimal DNA repair (PubMed:25329316). |
Cellular Location | Nucleus. Cytoplasm. Membrane. Mitochondrion. Note=Translocates to mitochondrion during apoptosis (By similarity). A small fraction localizes at membranes. Relocates to the cytoplasm when bound to STRAD (STRADA or STRADB) and CAB39/MO25 (CAB39/MO25alpha or CAB39L/MO25beta). PTEN promotes cytoplasmic localization (By similarity). |
Tissue Location | [Isoform 1]: Widely expressed. [Isoform 3]: Expressed in adult brain and liver and absent from tissues derived from postnatal day 7 |
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Background
Essential role in G1 cell cycle arrest. Phosphorylates and activates members of the AMPK-related subfamily of protein kinases (By similarity). Tumor suppressor.
References
Gao, Y., et al. Proc. Natl. Acad. Sci. U.S.A. 107(44):18892-18897(2010)
Bungard, D., et al. Science 329(5996):1201-1205(2010)
Koh, H.J., et al. Proc. Natl. Acad. Sci. U.S.A. 107(35):15541-15546(2010)
Foretz, M., et al. J. Clin. Invest. 120(7):2355-2369(2010)
Asada, N., et al. J. Neurosci. 30(26):8852-8865(2010)
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