BCL2 Interacting Killer Phospho-Thr33 (BIK pT33) Antibody
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Description
BIK (pT33) Antibody is a Rabbit Polyclonal against BIK (pT33).
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | BCL2 Interacting Killer Phospho-Thr33 (BIK pT33) |
| Host | Rabbit |
| Reactivity | Human |
| Assay Data | Modification: Phosphorylation // Target Modification: Thr33 |
| Recommended Dilution | ELISA: 1/10000, WB: 1/500 - 1/2000, IHC: 1/100 - 1/300. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Purified by affinity chromatography. |
| Size 1 | 50 µg |
| Size 2 | 100 µg |
| Form | Liquid |
| Tested Applications | ELISA, WB, IHC |
| Buffer | PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q13323 |
| Gene ID | 638 |
| Alias | BIP1,BP4,NBK,Apoptosis inducer NBK |
| Background | Antibody anti-BIK |
| Status | RUO |
Descripción
BIK is a pro-apoptotic member of the BCL-2 family that promotes programmed cell death by interacting with anti-apoptotic proteins, such as BCL-2 and BCL-XL, and neutralizing their function. BIK functions in the intrinsic apoptotic pathway, where it localizes to the mitochondria and induces mitochondrial outer membrane permeabilization (MOMP), leading to cytochrome c release and caspase activation. It acts as a BH3-only protein, a subclass of BCL-2 family proteins that serve as stress sensors for cellular damage, DNA replication errors, and oncogenic signaling. BIK is transcriptionally regulated by p53 and is involved in eliminating damaged or transformed cells, thus functioning as a tumor suppressor. BIK is often downregulated or silenced in cancers, where its loss contributes to apoptosis resistance, cell survival, and tumor progression. Overexpression studies show enhanced cell death, whereas knockdown studies reveal reduced apoptosis and increased tumor cell survival, highlighting BIK’s essential role in apoptosis induction, tumor suppression, and cellular stress responses.
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