Disease relevance of TAGLN3

• To gain an insight into the biological functions of NP25, we first examined its subcellular localization in the human neuroblastoma cell line, SK-N-SH [1].

High impact information on TAGLN3

• The results suggest that hNP22 may have a role in alcohol-related adaptations and may mediate regulatory signal transduction pathways in neurones [2].
• Sequence homology suggests a potential interaction of hNP22 with cytoskeletal elements. hNP22 mRNA was expressed in various brain regions but in alcoholics, greater mRNA expression occurred in the superior frontal cortex, but not in the primary motor cortex or cerebellum [2].
• Exercise also up-regulated specific synaptic-plasticity-related proteins, the cytoskeletal protein alpha-internexin and molecular chaperones (chaperonin-containing TCP-1, neuronal protein 22, heat shock 60-kDa protein 1 and heat shock protein 8) [3].
• Rat NP22 may affect microtubule or microfilament function, thereby regulating the neuroplastic changes associated with the development of alcohol dependence and physical withdrawal [4].
• Neuronal protein 22 colocalises with both the microtubule and microfilament cytoskeleton in neurite-like processes [5].

Biological context of TAGLN3

• The sequence of the NP25 cDNA reveals a single open reading frame that encodes a primary translation product of 206 amino acids [6].
• In contrast, a mutation to mimic persistent PKC phosphorylation resulted in a cellular morphology similar to that seen in wild-type hNP22 transfections [5].
• Transfection of mutant hNP22 containing either a deletion of the putative actin-binding domain or deletion of a consensus protein kinase C (PKC) phosphorylation site (Ser-180) failed to induce process formation [5].
• Further investigations using fluorescence resonance energy transfer (FRET) technique revealed intracellular binding of NP25 and actin [1].

Anatomical context of TAGLN3

• Expression of hNP22 is altered in the frontal cortex and hippocampus of the alcoholic human brain [7].
• Because previous studies have supported abnormalities in neuronal cytoarchitecture and/or development in the schizophrenia brain, we examined the expression of hNP22 in the anterior cingulate cortex, the hippocampus and the prefrontal cortex of schizophrenic and normal control postmortem brains using high-sensitive immunohistochemistry [8].
• Immunocytochemistry and in situ hybridization demonstrated that NP25 was differentially expressed by neuronal subpopulations of the rat central nervous system [6].
• It showed that NP25 co-localized with F-actin on stress fibers [1].

Associations of TAGLN3 with chemical compounds

• Fluoxetine treatment increased ERK2 and NP25 and decreased vacuolar ATP synthase [9].

Other interactions of TAGLN3

• Expression of human neuronal protein 22, a novel cytoskeleton-associated protein, was decreased in the anterior cingulate cortex of schizophrenia [8].

Analytical, diagnostic and therapeutic context of TAGLN3

• Molecular cloning and characterization of hNP22: a gene up-regulated in human alcoholic brain [2].
• Western blots revealed a significant increase in hNP22 protein levels in the frontal cortex but not the motor cortex of alcoholic cases [7].

References