Target type: biologicalprocess
Any process that activates or increases the frequency, rate, or extent of B cell apoptotic process. [GOC:add, GOC:mtg_apoptosis]
Positive regulation of B cell apoptotic process is a complex and tightly regulated process that ensures the removal of unwanted or potentially harmful B cells from the immune system. It is essential for maintaining immune homeostasis and preventing autoimmune diseases. The apoptotic pathway in B cells is triggered by a variety of stimuli, including signals from the B cell receptor (BCR), cytokines, and death receptors. These signals activate a cascade of intracellular events that lead to the activation of caspases, a family of proteases that execute the apoptotic program.
The positive regulation of B cell apoptosis is mediated by a variety of factors, including:
* **BCR signaling**: Engagement of the BCR by antigen can trigger apoptosis in B cells, especially if the antigen is presented in a non-productive manner or in the absence of appropriate co-stimulatory signals. This process involves the activation of various signaling pathways, including the MAPK and PI3K pathways, which ultimately lead to the activation of pro-apoptotic factors such as Bax and Bak.
* **Cytokine signaling**: Certain cytokines, such as TNF-α, can induce B cell apoptosis through the activation of death receptors, such as TNFR1. Activation of TNFR1 triggers a signaling cascade that culminates in the activation of caspases, leading to apoptosis.
* **Transcription factors**: Transcription factors, such as p53 and Foxo1, play important roles in regulating the expression of pro-apoptotic genes, contributing to the positive regulation of B cell apoptosis.
* **MicroRNAs**: MicroRNAs (miRNAs) are small non-coding RNAs that can regulate gene expression at the post-transcriptional level. Certain miRNAs have been implicated in the positive regulation of B cell apoptosis by targeting and inhibiting the expression of anti-apoptotic genes.
* **Other factors**: Other factors such as the expression of pro-apoptotic proteins like Bim and Puma, or the inactivation of anti-apoptotic proteins like Bcl-2 and Bcl-xL, also contribute to the positive regulation of B cell apoptosis.
The positive regulation of B cell apoptosis ensures the removal of potentially harmful or autoreactive B cells, preventing the development of autoimmune diseases. This process is carefully controlled to prevent excessive apoptosis that could lead to immune deficiencies. Dysregulation of B cell apoptosis can contribute to the development of various diseases, including autoimmune diseases, cancer, and infectious diseases.'
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Protein | Definition | Taxonomy |
---|---|---|
Apoptosis regulator BAX | An apoptosis regulator BAX that is encoded in the genome of human. [PRO:SY, UniProtKB:Q07812] | Homo sapiens (human) |
Interleukin-10 | An interleukin-10 that is encoded in the genome of human. [PRO:JAN, UniProtKB:P22301] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
vorinostat | vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL). Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME. | dicarboxylic acid diamide; hydroxamic acid | antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor |
abt-737 | aromatic amine; aryl sulfide; biphenyls; C-nitro compound; monochlorobenzenes; N-arylpiperazine; N-sulfonylcarboxamide; secondary amino compound; tertiary amino compound | anti-allergic agent; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor | |
hg-9-91-01 | HG-9-91-01 : A member of the class of phenylureas that is a potent inhibitor of salt-inducible kinase 2, a potential target protein for therapy in ovarian cancer. HG-9-91-01: inhibits salt-inducible kinases; structure in first source | aminopyrimidine; dimethoxybenzene; N-alkylpiperazine; N-arylpiperazine; phenylureas; secondary amino compound | antineoplastic agent; salt-inducible kinase 2 inhibitor |