Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Alpha (PIP5K1A) Antibody
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Description
PIP5K1A Antibody is a Rabbit Polyclonal Antibody against PIP5K1A.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Alpha (PIP5K1A) |
| Host | Rabbit |
| Reactivity | Human, Mouse |
| Recommended Dilution | ELISA: 1 µg/ml, WB: 1/500 - 1/2000, IHC-P: 1/50 - 1/200. Not tested in IHC-F. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Purified by affinity chromatography. |
| Size 1 | 20 µl |
| Size 2 | 100 µl |
| Size 3 | 2 × 100 µl |
| Form | Liquid |
| Tested Applications | ELISA, WB, IHC |
| Buffer | PBS, pH 7.3, containing 0.02% sodium azide, 50% glycerol. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q99755 |
| Gene ID | 8394 |
| NCBI Accession | NP_001129109.1 |
| Background | Antibody anti-PIP5K1A |
| Status | RUO |
| Note | Concentration: > 0.2 mg/ml - |
Descripción
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Overexpression of phosphatidylinositol phosphate 5-kinase alpha (PIP5KIalpha), which synthesizes PIP2, suppresses apoptosis, whereas a kinase-deficient mutant does not. Protection by the wild-type PIP5KIalpha isaccompanied by decreases in the generation of activated caspases and of caspase 3-cleaved PARP. Protection is not mediated through PIP3 or Akt activation. An anti-apoptotic role for PIP (2) is substantiated by the finding that PIP5KIalpha is cleaved by caspase 3 during apoptosis, and cleavage inactivates PIP5KIalpha in vitro. Mutation of the P (4) position (D279A) of the PIP5KIalpha caspase 3 cleavage consensus prevents cleavage in vitro, and during apoptosis in vivo. Significantly, the caspase 3-resistant PIP5KIalpha mutant is more effective in suppressing apoptosis than the wild-type kinase. PIP2 is a direct regulator of apical and effector caspases in the death receptor and mitochondrial pathways, and PIP5KIalpha inactivation contributes to the progression of apoptosis.
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