Foundational characteristics of cancer include proliferation, angiogenesis, migration, evasion of apoptosis, and cellular immortality. Find key markers for these cellular processes and antibodies to detect them.
The SUMOplot™ Analysis Program predicts and scores sumoylation sites in your protein. SUMOylation is a post-translational modification involved in various cellular processes, such as nuclear-cytosolic transport, transcriptional regulation, apoptosis, protein stability, response to stress, and progression through the cell cycle.
The Autophagy Receptor Motif Plotter predicts and scores autophagy receptor binding sites in your protein. Identifying proteins connected to this pathway is critical to understanding the role of autophagy in physiological as well as pathological processes such as development, differentiation, neurodegenerative diseases, stress, infection, and cancer.
TIGAR Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9NQ88 |
|---|---|
| Clone Names | 110901196 |
| Gene ID | 57103 |
|---|---|
| Other Names | Fructose-2, 6-bisphosphatase TIGAR, TP53-induced glycolysis and apoptosis regulator, TIGAR, C12orf5 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | TIGAR {ECO:0000303|PubMed:16839880} |
|---|---|
| Synonyms | C12orf5 |
| Function | Fructose-bisphosphatase hydrolyzing fructose-2,6-bisphosphate as well as fructose-1,6-bisphosphate (PubMed:19015259). Acts as a negative regulator of glycolysis by lowering intracellular levels of fructose-2,6-bisphosphate in a p53/TP53-dependent manner, resulting in the pentose phosphate pathway (PPP) activation and NADPH production (PubMed:16839880, PubMed:22887998). Contributes to the generation of reduced glutathione to cause a decrease in intracellular reactive oxygen species (ROS) content, correlating with its ability to protect cells from oxidative or metabolic stress-induced cell death (PubMed:16839880, PubMed:19713938, PubMed:23726973, PubMed:22887998, PubMed:23817040). Plays a role in promoting protection against cell death during hypoxia by decreasing mitochondria ROS levels in a HK2- dependent manner through a mechanism that is independent of its fructose-bisphosphatase activity (PubMed:23185017). In response to cardiac damage stress, mediates p53-induced inhibition of myocyte mitophagy through ROS levels reduction and the subsequent inactivation of BNIP3. Reduced mitophagy results in an enhanced apoptotic myocyte cell death, and exacerbates cardiac damage (By similarity). Plays a role in adult intestinal regeneration; contributes to the growth, proliferation and survival of intestinal crypts following tissue ablation (PubMed:23726973). Plays a neuroprotective role against ischemic brain damage by enhancing PPP flux and preserving mitochondria functions (By similarity). Protects glioma cells from hypoxia- and ROS- induced cell death by inhibiting glycolysis and activating mitochondrial energy metabolism and oxygen consumption in a TKTL1- dependent and p53/TP53-independent manner (PubMed:22887998). Plays a role in cancer cell survival by promoting DNA repair through activating PPP flux in a CDK5-ATM-dependent signaling pathway during hypoxia and/or genome stress-induced DNA damage responses (PubMed:25928429). Involved in intestinal tumor progression (PubMed:23726973). |
| Cellular Location | Cytoplasm. Nucleus Mitochondrion. Note=Translocated to the mitochondria during hypoxia in a HIF1A-dependent manner (PubMed:23185017). Colocalizes with HK2 in the mitochondria during hypoxia (PubMed:23185017). Translocated to the nucleus during hypoxia and/or genome stress-induced DNA damage responses in cancer cells (PubMed:25928429). Translocation to the mitochondria is enhanced in ischemic cortex after reperfusion and/or during oxygen and glucose deprivation (OGD)/reoxygenation insult in primary neurons (By similarity). {ECO:0000250|UniProtKB:Q8BZA9, ECO:0000269|PubMed:23185017, ECO:0000269|PubMed:25928429} |
| Tissue Location | Expressed in the brain (PubMed:22887998). Expressed in breast tumors (PubMed:21820150). Expressed in glioblastomas (PubMed:22887998). |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
info@abcepta.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
Background
This gene is regulated as part of the p53 tumor suppressorpathway and encodes a protein with sequence similarity to thebisphosphate domain of the glycolytic enzyme that degradesfructose-2,6-bisphosphate. The protein functions by blockingglycolysis and directing the pathway into the pentose phosphateshunt. Expression of this protein also protects cells from DNAdamaging reactive oxygen species and provides some protection fromDNA damage-induced apoptosis. The 12p13.32 region that includesthis gene is paralogous to the 11q13.3 region. [provided byRefSeq].
References
Bensaad, K., et al. EMBO J. 28(19):3015-3026(2009)Trevino, L.R., et al. Nat. Genet. 41(9):1001-1005(2009)Lopez-Guerra, M., et al. Haematologica 93(12):1843-1851(2008)Matsuoka, S., et al. Science 316(5828):1160-1166(2007)Bensaad, K., et al. Cell 126(1):107-120(2006)
If you have used an Abcepta product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at tech@abcepta.com.
Ordering Information
Other Products
Shipping Information
