MAP1B and Associated Diseases
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Backgrounds of MAP1B
Microtubule-associated protein 1B (MAP1B) is a protein complex composed of a heavy chain and a light chain (LC1). It plays an important role in the stability of the cytoskeleton and may have other cellular functions and is a neural-specific microtubule-associated protein that is the first MAP expressed by neurons in situ and present in axons, somata, and dendrites. MAP1B was identified as a membrane glycoprotein that localized to the global membrane protein of the neuronal vesicles and plasma membrane. MAP1B is highly expressed in the early stage of neuronal development and gradually decreases during maturation. It is expressed at high levels in the brain and the spinal cord, and at much lower levels in muscle, predominantly during the early stages of the nervous system development where it regulates processes such as microtubule and actin dynamics. Similar to MAP1S, MAP1A and MAP1B are thought to play an important role in regulating mitochondrial dynamics and cell death.
Functions of MAP1B
MAP1B encodes for microtubule-associated protein 1B, one of the major cytoskeletal proteins that are involved in various cellular activities including actin-based cell motility, molecular trafficking, autophagy, and cancer. MAP1B is involved in many cellular functions. It promotes microtubule assembly and is essential for neuronal process differentiation and the growth and maintenance of LTP. The interaction between MAP1B and the disease-associated protein gigaxonin is thought to play an important role in the progression of giant axonal neuropathy, a human neurodegenerative disease.
Fig.1 Model for MAP1B-LC1/UBE2L3-mediated CaV2 channel regulation. (Gandini, 2014)
Expression of MAP1B in Diseases
MAP1B is considered to be an important regulator of axon and dendrite growth and guidance. It was shown that regenerating neurons in MAP1B-deficient mice exhibited defects in axonal branching and growth cone motility, also apparently due to a disruption of normal cytoskeletal dynamics. MAP1B mutations have recently been associated with a phenotype that includes periventricular nodular ectopic (PVNH), intellectual disability (ID), epilepsy, and malformation features. The loss of MAP1B function resulted in the inhibition of neurite outgrowth and cell death pointing to the fact that MAP1B function cannot be fully compensated by other MAPs.
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Reference
- Gandini, M.A.; et al. The MAP1B-LC1/UBE2L3 complex catalyzes the degradation of cell surface CaV2. 2 channels. Channels. 2014, 8(5): 452-457.
