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  Indian J Med Microbiol
 

Figure 2: Loss of FEZ1 function is implicated in neurodegeneration. (1) The loss of FEZ1 function causes perturbations in axonal transport, leading to the build-up of stranded cargoes along with unphosphorylated FEZ1 aggregates. (2) Disrupted axonal transport blocks synaptic cargo delivery, which in turn, affects synaptic function. (3) Neurodegenerative phenotypes are commonly associated with intracellular protein aggregates. Autophagy is a catabolic process often upregulated under neurodegenerative conditions in order to remove these aggregates. FEZ1 is a regulator of autophagy via its interaction with various proteins such as ULK1, SCOC and UVRAG. FEZ1: Fasciculation and elongation protein zeta-1; SCOC: short coiled coil protein; ULK1: UNC-51-like kinase; UVRAG: ultraviolet radiation resistance associated gene. Image was created using Biorender graphic software (https://biorender.com/).

<b>Figure 2: Loss of FEZ1 function is implicated in neurodegeneration.</b>
(1) The loss of FEZ1 function causes perturbations in axonal transport, leading to the build-up of stranded cargoes along with unphosphorylated FEZ1 aggregates. (2) Disrupted axonal transport blocks synaptic cargo delivery, which in turn, affects synaptic function. (3) Neurodegenerative phenotypes are commonly associated with intracellular protein aggregates. Autophagy is a catabolic process often upregulated under neurodegenerative conditions in order to remove these aggregates. FEZ1 is a regulator of autophagy via its interaction with various proteins such as ULK1, SCOC and UVRAG. FEZ1: Fasciculation and elongation protein zeta-1; SCOC: short coiled coil protein; ULK1: UNC-51-like kinase; UVRAG: ultraviolet radiation resistance associated gene. Image was created using Biorender graphic software (<a target=https://biorender.com/).">