PDLIM2 Antibody, FITC conjugated
Description
Cancer Biology
PDLIM2 functions as a tumor suppressor by repressing STAT3 and NF-κB signaling pathways. Studies using PDLIM2 antibodies, including FITC-conjugated variants, have revealed:
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Lung Cancer: PDLIM2 downregulation in alveolar macrophages promotes STAT3-driven immunosuppression and lung tumor progression . Epigenetic restoration of PDLIM2 enhances chemotherapy sensitivity and synergizes with anti-PD-1 therapy .
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Lymphoma: Loss of PDLIM2 expression in classical Hodgkin lymphoma (cHL) correlates with constitutive activation of pro-survival transcription factors like NF-κB and STAT3 .
Immune Regulation
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T-Cell Leukemia: PDLIM2 induces K48-linked ubiquitination and degradation of the HTLV-I Tax oncoprotein, suppressing viral oncogenesis .
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Macrophage Polarization: PDLIM2 deficiency in alveolar macrophages increases monocyte recruitment and protumorigenic polarization, contributing to lung cancer immune evasion .
Mechanism of Action
PDLIM2 operates through:
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Ubiquitin E3 Ligase Activity: Targets STAT3, RelA, and Tax for proteasomal degradation .
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Epigenetic Regulation: Repressed in cancer via ROS-activated BACH1 or promoter hypermethylation, linking it to poor prognosis .
Therapeutic Implications
Comparative Analysis of PDLIM2 Antibodies
| Feature | FITC-Conjugated (CSB-PA856962LC01HU) | Unconjugated (ab246868) |
|---|---|---|
| Detection Method | Fluorescence-based assays | Western blot, IHC, ICC/IF |
| Sensitivity | High (1:20 dilution for IHC) | Moderate (1:100–1:1000 dilution) |
| Applications | IF, ELISA | WB, IHC, ICC |
Limitations and Future Directions
While FITC-conjugated PDLIM2 antibodies are critical for fluorescence-based studies, their utility in multiplex assays is limited compared to newer conjugates (e.g., HRP or biotin). Ongoing research focuses on:
Product Specs
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
PDLIM2 is a probable adapter protein localized to the actin cytoskeleton, facilitating cell adhesion. It is essential for epithelial cell migration. Overexpression enhances cell adhesion to collagen and fibronectin while suppressing anchorage-independent growth, suggesting a potential role in regulating tumor cell migratory capacity.
Further research indicates the following roles for PDLIM2:
- Surface plasmon resonance (SPR) chip-based analysis yielded comparable data to streptavidin bead methods. Gravity flow/microflow washing and elution proved superior to centrifugation. Detergent type and concentration minimally impacted cancer-associated PDLIM2 interactome data. (PMID: 30194080)
- PDLIM2 inactivation is frequently observed in classical Hodgkin lymphoma (cHL) and anaplastic large cell lymphoma (ALCL), promoting inflammatory signaling and contributing to pathogenesis. (PMID: 27538486)
- PDLIM2 knockdown significantly reduces cellular proliferation in primary meningioma and schwannoma. (PMID: 28126595)
- PDLIM2 is epigenetically repressed in ovarian cancer. Its inhibition promotes tumor growth in vivo and in vitro via NOS2-derived nitric oxide signaling, recruiting M2 type macrophages. (PMID: 26593252)
- PDLIM2 suppression significantly reduces cell proliferation, growth, and invasiveness in prostate cancer cells. (PMID: 26499308)
- Epigenetic repression of PDLIM2 can be reversed by 5-aza-2'-deoxycytidine and vitamin D, suppressing KSHV-associated cancer cell growth. (PMID: 25681443)
- PDLIM2 is crucial for feedback regulation of the β1-integrin-RhoA signaling axis, integrating microenvironment signals with gene expression to control breast epithelial acini polarity. (PMID: 24863845)
- PDLIM2 integrates cytoskeleton signaling with gene expression in epithelial differentiation, controlling the stability of key transcription factors and COP9 signalosome activity. (PMID: 24196835)
- PDLIM2 is a direct target gene of 1,25(OH)2D3. (PMID: 23584482)
- Pdlim2 is a novel actin-regulating protein in podocyte foot processes, potentially involved in glomerular disease pathogenesis. (PMID: 21814175)
- PDLIM2 directly binds to Tax via a putative alpha-helix motif (amino acids 236-254). (PMID: 20838382)
- PDLIM2, a key NF-κB activation terminator, is repressed in ER-positive and ER-negative breast cancer cells, explaining constitutive NF-κB activation. (PMID: 20185823)
- PDLIM2 repression is independent of the viral regulatory protein Tax. (PMID: 19794962)
- Mystique 2 (PDLIM2) siRNA knockdown abrogates adhesion and migration in MCF10A and MCF-7 cells. (PMID: 15659642)
- PDLIM2 deficiency leads to increased nuclear p65, defective p65 ubiquitination, and augmented proinflammatory cytokine production. (PMID: 17468759)
- PDLIM2 suppression reduces cell adhesion, increases NF-κB transcription reporter activity, and enhances LPS-induced TNF-α production. (PMID: 19052146)
