PKS1 operates in two primary pathways:
A. Phototropin Signaling
Mediates phot1-dependent hypocotyl phototropism under low-fluence blue light .
Genetic studies show redundancy with PKS2 and PKS4; triple mutants (pks1/pks2/pks4) exhibit severe phototropic defects .
Part of the Very Low Fluence Response (VLFR) branch of phyA signaling .
Regulates hypocotyl growth inhibition and cotyledon expansion .
The PKS1 antibody has enabled critical discoveries through:
Specificity: No cross-reactivity with PKS2 or PKS4, confirmed using pks1/pks2/pks4 mutants .
Utility: Used to track PKS1 induction under white light (4-hour exposure) .
PKS1 antibody studies have clarified:
Here’s a structured collection of FAQs tailored for academic researchers working with the KS1/4 antibody (note: "PKS1" may refer to a typographical error; the sources reference KS1/4 antibody conjugates):
Target downregulation: Observed in HER2 ADCs; monitor antigen loss via sequential biopsies or liquid biopsies .
Drug efflux pumps: Overexpression of ABC transporters (e.g., ABCB1) reduces intracellular methotrexate accumulation. Test with verapamil co-treatment .
Immune evasion: HAMA responses neutralize conjugate efficacy. Use humanized antibody formats or immunosuppressive adjuvants .
Synergy rationale:
Trial design: Phase Ib/II studies using KS1/4-methotrexate + checkpoint inhibitors, stratified by PD-L1 status .
Molecular docking: Use RosettaAntibody or AlphaFold-Multimer to model KS1/4-antigen binding.
MD simulations: Assess conformational stability of the antibody-antigen complex under physiological conditions.
Validation: Cross-reference with mutagenesis data (e.g., alanine scanning) from NSCLC cell lines .