Control of apoptosis by SMAR1
Md Zubbair Malik1, Md Jahoor Alam2, Romana Ishrat3
1Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi-110025, India and School of Computational and Integrative Sciences, Jawaharlal Nehru University, New Delhi-110067, India. brojen@jnu.ac.in.
Molecular Biosystems
|December 10, 2016
Summary
Nuclear matrix-associated protein SMAR1 regulates p53 dynamics and cellular states under stress. Its stress-induced fractal behavior in networks optimizes information flow and aids stress management.
Area of Science:
- Cellular biology
- Systems biology
- Network biology
Background:
- Nuclear matrix-associated protein SMAR1 is a key regulator in the p53 network.
- SMAR1's role in stress response and its impact on p53 dynamics are not fully understood.
Purpose of the Study:
- To investigate how SMAR1 modulates p53 dynamics under varying stress conditions.
- To analyze the fractal and topological properties of cellular networks influenced by SMAR1 and stress.
Main Methods:
- Analysis of p53 dynamics under different stress levels induced by SMAR1.
- Construction and topological analysis of networks based on p53 dynamical states.
- Investigation of SMAR1's interaction with HDAC1 in apoptosis regulation.
Main Results:
- SMAR1 drives p53 dynamics into distinct states corresponding to cellular states, exhibiting multifractal behavior.
- Fractal network properties indicate self-organization for optimized information flow.
- Network assortativity highlights the role of time-series hubs in stress management.
Conclusions:
- SMAR1 acts as a stress inducer and regulator, influencing p53 network dynamics and cellular states.
- The observed fractal and topological network characteristics are signatures of self-organization and efficient stress response.
- SMAR1's regulation of apoptosis, in conjunction with HDAC1, is stress-dependent.
Related Concept Videos
The Intrinsic Apoptotic Pathway
9.0K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.0K
The Extrinsic Apoptotic Pathway
9.1K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.1K
Apoptosis
16.5K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
16.5K
Caspases
14.4K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
14.4K
Abnormal Proliferation
5.4K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.4K
Phagocytosis of Apoptotic Cells
5.4K
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized...
Normal cells contain receptors that prevent them from being recognized...
5.4K


