kpc-1 Antibody
Description
Molecular Function and Targets
KPC1 regulates protein degradation via the ubiquitin-proteasome system (UPS), primarily targeting:
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NF-κB1 p105: Processes it into the active p50 subunit, modulating NF-κB signaling .
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p27: Promotes cytoplasmic ubiquitination and degradation, influencing cell cycle progression .
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Bax: Facilitates proteasomal degradation to mitigate apoptosis under stress conditions .
In pancreatic ductal adenocarcinoma (PDAC) models (e.g., KPC mice), KPC1 expression correlates with immune microenvironment dynamics, including T-cell infiltration and myeloid cell modulation .
Oncogenic and Tumor-Suppressive Contexts
Cardioprotective Role
Antibody-Drug Conjugates (ADCs)
A study targeting urokinase plasminogen activator receptor (uPAR) with FL1-PNU ADC in PDAC models revealed:
| Cell Line | uPAR Expression (per cell) | FL1-PNU EC50 (nM) | Selectivity Index |
|---|---|---|---|
| MDA-MB-231 | 1.3 × 10⁶ | 0.005 | 3600 |
| KPC1 (uPAR KO) | 4.4 × 10² | 17 | 2 |
FL1-PNU reshaped the tumor microenvironment (TME), reducing immunosuppressive myeloid cells and enhancing CD8+ T-cell infiltration .
Immune Checkpoint Modulation
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In KPC mice, combined PD-1/PD-L1 blockade increased TNFα+ T cells and eradicated tumors in 50% of cases .
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KPC1-deficient tumors exhibited reduced MHC class I expression, enabling immune evasion .
Epigenetic Regulation
Neuronal Guidance
Technical Use Cases for KPC-1 Antibodies
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Co-Immunoprecipitation: Anti-KPC1 (sc-101122, Santa Cruz) validated interactions with Bax in cardiac cells .
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Western Blotting: Detected KPC1 upregulation in H/R-treated H9c2 cells (1.5-fold increase vs. control) .
Clinical Implications
Product Specs
Components: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
The kpc-1 antibody targets KPC-1, a furin-like protease in Caenorhabditis elegans. This protease cleaves proproteins at the RX(K/R)R consensus motif. During neuronal development, KPC-1 critically regulates dendrite branch formation and extension, as well as neuronal positioning. In conjunction with CHIN-1 and CDC-42, it plays a crucial role in neuropil development and axon guidance, particularly for axons from SubL pioneer neurons and AIY interneurons into the nerve ring. Its influence on axon guidance in glia and pioneer neurons may involve the proper localization of FMI-1 protein to the nerve ring. KPC-1 promotes the formation, extension, and self-avoidance of dendritic branches in PVD and FLP mechanosensory neurons. In PVD neurons, it regulates plasma membrane levels of the branching receptor DMA-1 by targeting it to late endosomes, thereby promoting normal dendrite branching and self-avoidance. Further, KPC-1 controls dendrite extension in AIY and D-type motoneurons, dendrite branching in AQR sensory neurons and VC4/5 motoneurons, the number of dendritic branches in AVL neurons, and the positioning of HSN and ALM/PLM neurons. While dispensable for maintaining adult dendrite branching, it regulates dauer-specific dendritic branching of IL2 neurons and dauer-specific nictation behavior. Under stressful environmental conditions, KPC-1 may promote dauer formation by processing insulin-like proteins INS-1 and INS-18, two antagonists of DAF-2/InsR.
- A chin-1 (Chimaerin) and kpc-1 (Furin) double mutant severely disrupts neuronal assembly. CHIN-1 and KPC-1 function non-canonically in glia and pioneer neurons for guidance-cue trafficking. PMID: 28846083
- KPC-1 regulates the dendritic level of the branching receptor DMA-1 by targeting it to late endosomes. PMID: 26974341
- KPC-1 is required for dauer IL2 dendritic arborization and dauer-specific nictation behavior, and is also necessary for dendritic arborization of PVD and FLP sensory neurons. PMID: 23932402
