| Host: |
Rabbit |
| Applications: |
IHC/WB |
| Reactivity: |
Human/Mouse |
| Note: |
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
| Short Description: |
Rabbit polyclonal antibody anti-Phospho-Death-associated protein kinase 1-Ser289 is suitable for use in Immunohistochemistry and Western Blot research applications. |
| Clonality: |
Polyclonal |
| Conjugation: |
Unconjugated |
| Isotype: |
IgG |
| Formulation: |
Liquid in PBS containing 50% Glycerol and 0.02% Sodium Azide. |
| Purification: |
The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen. |
| Concentration: |
1 mg/mL |
| Dilution Range: |
WB 1:500-2000IHC 1:50-200 |
| Storage Instruction: |
Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles. |
| Gene Symbol: |
DAPK1 |
| Gene ID: |
1612 |
| Uniprot ID: |
DAPK1_HUMAN |
| Specificity: |
This antibody detects endogenous levels of DAPK1 (Phospho Ser289) Rabbit pAb at Human, Mouse |
| Immunogen: |
Synthesized peptide derived from human DAPK1 (Phospho Ser289) |
| Tissue Specificity | Isoform 2 is expressed in normal intestinal tissue as well as in colorectal carcinomas. |
| Post Translational Modifications | Ubiquitinated by the BCR(KLHL20) E3 ubiquitin ligase complex, leading to its degradation by the proteasome. Removal of the C-terminal tail of isoform 2 (corresponding to amino acids 296-337 of isoform 2) by proteolytic cleavage stimulates maximally its membrane-blebbing function. In response to mitogenic stimulation (PMA or EGF), phosphorylated at Ser-289.phosphorylation suppresses DAPK1 pro-apoptotic function. Autophosphorylation at Ser-308 inhibits its catalytic activity. Phosphorylation at Ser-734 by MAPK1 increases its catalytic activity and promotes cytoplasmic retention of MAPK1. Endoplasmic-stress can cause dephosphorylation at Ser-308. |
| Function | Calcium/calmodulin-dependent serine/threonine kinase involved in multiple cellular signaling pathways that trigger cell survival, apoptosis, and autophagy. Regulates both type I apoptotic and type II autophagic cell deaths signal, depending on the cellular setting. The former is caspase-dependent, while the latter is caspase-independent and is characterized by the accumulation of autophagic vesicles. Phosphorylates PIN1 resulting in inhibition of its catalytic activity, nuclear localization, and cellular function. Phosphorylates TPM1, enhancing stress fiber formation in endothelial cells. Phosphorylates STX1A and significantly decreases its binding to STXBP1. Phosphorylates PRKD1 and regulates JNK signaling by binding and activating PRKD1 under oxidative stress. Phosphorylates BECN1, reducing its interaction with BCL2 and BCL2L1 and promoting the induction of autophagy. Phosphorylates TSC2, disrupting the TSC1-TSC2 complex and stimulating mTORC1 activity in a growth factor-dependent pathway. Phosphorylates RPS6, MYL9 and DAPK3. Acts as a signaling amplifier of NMDA receptors at extrasynaptic sites for mediating brain damage in stroke. Cerebral ischemia recruits DAPK1 into the NMDA receptor complex and it phosphorylates GRINB at Ser-1303 inducing injurious Ca(2+) influx through NMDA receptor channels, resulting in an irreversible neuronal death. Required together with DAPK3 for phosphorylation of RPL13A upon interferon-gamma activation which is causing RPL13A involvement in transcript-selective translation inhibition. Isoform 2 cannot induce apoptosis but can induce membrane blebbing. |
| Protein Name | Death-Associated Protein Kinase 1Dap Kinase 1 |
| Database Links | Reactome: R-HSA-418889 |
| Cellular Localisation | Isoform 1: CytoplasmCytoplasmCytoskeletonColocalizes With Map1b In The Microtubules And Cortical Actin FibersIsoform 2: Cytoplasm |
| Alternative Antibody Names | Anti-Death-Associated Protein Kinase 1 antibodyAnti-Dap Kinase 1 antibodyAnti-DAPK1 antibodyAnti-DAPK antibody |
Information sourced from Uniprot.org
12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance
