Which of the following prevents memory B cells from apoptosis
NGF can drive the expression of genes such as bcl-2by binding to the TrkA receptor, which stimulates the proliferation and survival of the target neuron. High affinity binding between proNGF, soilin, and p75NTR can result in either survival or programmed cell death. Study results indicate that superior cervical ganglia neurons that express both p75NTR and TrkA die when treated with proNGF, while NGF treatment of these same neurons results in survival and axonal growth. Survival and PCD mechanisms are mediated through adaptor protein binding to the death domain of the p75NTR cytoplasmic tail. Survival occurs when recruited cytoplasmic adaptor proteins facilitate signal transduction through tumor necrosis factor receptor members such as TRAF6, which results in the release of nuclear factor kB (NF-kB) transcription activator. NF-kB regulates nuclear gene transcription to promote cell survival. Alternatively, programmed cell death occurs when TRAF6 and neurotrophin receptor interacting factor (NRIF) are both recruited to activate c-Jun N-terminal kinase (JNK); which phosphorylates c-Jun. The activated transcription factor c-Jun regulates nuclear transcription AP-1 to increase pro-apoptotic gene transcription Ref Robbins 9/e p16
PDGF
Nerve growth factor
Insulin like growth factor
Fibroblast growth factor
General pathology