Frederick W. Alt

The paper demonstrates that a human antibody heavy chain variable region exon forms a stable somatic hypermutation center (SHM-C) through interaction with 3' regulatory regions, supporting AID access and SHM in non-dividing cells.

The paper shows that B cell receptor signaling sets limits on the selection of functional mutations in antibodies, with mid-affinity antigens showing optimal neutralization.

The paper shows that boosting at the same site as the initial immunization preferentially engages bnAb lineage precursors in secondary germinal centers, while contralateral boosting recruits naive and non-specific memory B cells.

This paper develops six mouse models with engineered antibody repertoires to study and optimize strategies for inducing HIV-1 broadly neutralizing antibodies.

This paper develops a mouse model to study and overcome challenges in maturing HIV-1 broadly neutralizing antibodies by expressing a stalled VRC01 intermediate in germinal center B cells.

This study uses molecular dynamics simulations to design HIV-1 immunogens that select for specific mutations in broadly neutralizing antibodies.

The paper shows that Ku70 suppresses alternative end-joining (A-EJ) in G1-arrested progenitor B cells, directing DSB repair toward classical nonhomologous end-joining (C-NHEJ) and preventing translocations.

The paper investigates RDC-gene breakage in neural progenitor cells derived from embryonic stem cells, finding that many RDCs in primary NSPCs are developmentally influenced and appear in cultured NPCs.