Anti-RPT1 (aa 1-100) polyclonal antibody

Elective neck dissection in patients with recurrent head and neck squamous cell carcinoma (HNSCC) without evidence of neck disease (crN0) is poorly defined. A retrospective review was carried out on 165 crN0 patients treated with salvage surgery and elective neck dissection. Multivariate Cox analysis and recursive partitioning analysis were used to evaluate prognostic factors. The frequency of occult neck node metastases in the neck dissection (rpN+) was 16.4%. The risk of occult metastases for glottic rpT1-T2 recurrences was 5.9%, for glottic rpT3-T4 recurrences 13.2%, for non-glottic rpT1-T2 recurrences 16.1% and for locally advanced ( rpT3-T4) non-glottic recurrences 31.1%. Patients with occult neck node metastases (rpN+) had a 5-year adjusted survival rate of 38.1%, while patients without nodal disease (rpN0) had a 5-year adjusted survival rate of 71.1% (p = 0.0001). Elective neck dissection can be omitted in crN0 patients with rT1-T2 glottic recurrence. We consider it advisable to perform elective neck dissection in all other situations.

The regulatory particle (RP) of the 26S proteasome contains a heterohexameric ring of AAA-ATPases (RPT1-6) that unfolds and inserts substrates into the core protease (CP) for degradation. Through genetic analysis of the Arabidopsis thaliana gene pair encoding RPT2, we show that this subunit plays a critical role in 26S proteasome assembly, histone dynamics, and plant development. rpt2a rpt2b double null mutants are blocked in both male and female gamete transmission, demonstrating that the subunit is essential. Whereas rpt2b mutants are phenotypically normal, rpt2a mutants display a range of defects, including impaired leaf, root, trichome, and pollen development, delayed flowering, stem fasciation, hypersensitivity to mitomycin C and amino acid analogs, hyposensitivity to the proteasome inhibitor MG132, and decreased 26S complex stability. The rpt2a phenotype can be rescued by both RPT2a and RPT2b, indicative of functional redundancy, but not by RPT2a mutants altered in ATP binding/hydrolysis or missing the C-terminal hydrophobic sequence that docks the RPT ring onto the CP. Many rpt2a phenotypes are shared with mutants lacking the chromatin assembly factor complex CAF1. Like caf1 mutants, plants missing RPT2a or reduced in other RP subunits contain less histones, thus implicating RPT2 specifically, and the 26S proteasome generally, in plant nucleosome assembly.