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The β-H elimination, as one of the most important elementary reactions in transition metal chemistry, is a key step in quenching the carbon-palladium bond for the Heck reaction. However, the β-H elimination of the alkenyl palladium species leading to allene is an energetically unfavored process, and therefore, it has been a long-standing challenge in control of this process via enantioselective manner. We developed a concise and efficient methodology to construct trisubstituted chiral allenes from stereodefined fully substituted enol triflates by the enantioselective β - H elimination of the alkenyl palladium species under mild conditions. The identified Xu-Phos play a crucial role in the chemoselectivity and enantioselectivity. Multiple linear regression analysis shows the important steric effect on enantioselectivity. DFT computation results allow us to propose an intramolecular base ( − OAc)–assisted deprotonation mechanism for this progress. Distortion-interaction and energy decomposition analysis indicate that the difference in electrostatic energy ( E elec ) of the two intramolecular base-assisted deprotonation transition states dominates the stereoselectivity.

c-Cbl suppresses RelB activation to facilitate protective benefits of commensal fungi and maintain intestinal homeostasis., Intestinal fungi are critical for modulating host immune homeostasis and underlying mechanisms remain unclear. We show that dendritic cell (DC)–specific deficiency of casitas B-lineage lymphoma (c-Cbl) renders mice susceptible to dextran sodium sulfate (DSS)–induced colitis. Mechanistically, we identify that c-Cbl functions downstream of Dectin-2 and Dectin-3 to mediate the ubiquitination and degradation of noncanonical nuclear factor κB subunit RelB. Thus, c-Cbl deficiency in DCs promotes α-mannan–induced activation of RelB, which suppresses p65-mediated transcription of an anti-inflammatory cytokine gene, il10, thereby aggravating DSS-induced colitis. Moreover, suppressing fungal growth with fluconazole or inhibition of RelB activation in vivo attenuates colitis in mice with DC-specific deletion of c-Cbl. We also demonstrate an interaction between c-Cbl and c-Abl tyrosine kinase and find that treatment with DPH, a c-Abl agonist, synergistically increases fungi-induced c-Cbl activation to restrict colitis. Together, these findings unravel a previously unidentified fungi-induced c-Cbl/RelB axis that sustains intestinal homeostasis and protects against intestinal inflammation.