Isolation or enrichment of biological molecules from complex biological samples is mostly a prerequisite in proteomics, genomics, and glycomics. Different techniques have been used to advance the efficiency of the purification of biological molecules. Bioaffinity chromatography is one of the most powerful technique that plays an important role in the isolation of target biological molecules by the specific interactions with ligands that are immobilized on different support materials. This review examines the recent developments in bioaffinity chromatography particularly over the past 5 years in the literature. Also properties of supports, immobilization techniques, types of binding agents, and methods used in bioaffinity chromatography applications are summarized.

Recent trends in sorbents for bioaffinity chromatography.

OBJECTIVES
The co-occurrence of melanoma and Parkinson's disease (PD) is higher than expected. We review the relationship between melanoma and PD, then proffer a hypothesis of how dysregulated human tyrosinase could be involved in both diseases via the loss of dopamine and neuromelanin-positive neurons in PD and the genesis alterations in melanin content during melanoma.


KEY FINDINGS
There are a surprising number of links between skin disorders and neurodegenerative diseases. Some risk factors related to the co-occurrence of PD and melanoma have been extensively investigated over the past 15 years. It has been proposed that human tyrosinase, an enzyme participating in the biosynthesis of neuromelanin in the brain and of melanin in the skin, plays a role. Abnormally dysregulated human tyrosinase impacts the genesis and progression of melanoma and PD.


SUMMARY
The dual role of human tyrosinase places it as the potential critical link between these seemingly distinct conditions. Detecting and monitoring human tyrosinase activity in the progression of melanoma and PD opens new opportunities for early diagnosis and treatment of both diseases.

Dysregulation of tyrosinase activity: a potential link between skin disorders and neurodegeneration.

Restoration of metal homeostasis: a potential strategy against neurodegenerative diseases

Facile synthesis of bifunctional polymer monolithic column for tunable and specific capture of glycoproteins and phosphoproteins.

The last ten years have witnessed the increasingly notable advances in immobilized metal ion chromatography (IMAC) for phosphoproteomic profiling. Protein phosphorylation is an important post-translational modification (PTM) that participates in multiple cellular processes. Phosphoproteomics provides powerful analysis and unique insights for the study of phosphorylation-related cellular processes and disease mechanisms. IMAC enrichment strategy could capture phosphopeptides with chemical interaction between the phosphoamino acids and the immobilized metal cations. Currently, IMAC materials and workflows have matured and are applied in capturing phosphopeptides at substoichiometric levels. The design of IMAC enrichment materials and matching workflows are particularly vital in phosphoproteomic profiling. This review mainly focuses on overviewing present advances in the materials, workflows, and applications of immobilized metal ion chromatography for phosphoproteomic profiling, including a brief discussion on their advantages, current challenges, and trends in the future development. 

Materials, workflows and applications of IMAC for phosphoproteome profiling in the recent decade: A review

Affinity chromatography assisted comprehensive phosphoproteomics analysis of human saliva for lung cancer

Background Dilated cardiomyopathy (DCM), which is a major cause of heart failure, is a primary cardiac muscle disease with high morbidity and mortality rates. DCM is a genetically heritable disease and more than 10 gene ontologies have been implicated in DCM. CDH2 encodes N-cadherin and belongs to a superfamily of transmembrane proteins that mediate cell–cell adhesion in a calcium-dependent manner. Deficiency of CDH2 is associated with arrhythmogenic right ventricular cardiomyopathy (OMIM: 618920) and agenesis of the corpus callosum, cardiac, ocular, and genital syndrome (OMIM: 618929). However, there have been no reports of isolated DCM associated with CDH2 deficiency. Methods We performed whole exome sequencing in a 12-year-old girl with non-syndromic DCM and her unaffected parents. Variants in both known DCM-related genes and novel candidate genes were analyzed and pathogenicity confirmation experiments were performed. Results No pathogenic/likely pathogenic variant in known DCM-related genes was identified in the patient. We found a de novo variant in a candidate gene CDH2 in the patient, namely, c.474G>C/p.Lys158Asn (NM_001792.5). This variant has not been reported in the ClinVar or Human Gene Mutation Database (HGMD). CDH2 p.Lys158Asn was found in the conserved domain of N-cadherin, which is associated with the hydrolysis of the precursor segment and interference with adhesiveness. Furthermore, we tested the expression and efficiency of cell–cell adhesion while overexpressing the CDH2 Lys158Asn mutant and two previously reported variants in CDH2 as positive controls. The adhesion efficiency was considerably reduced in the presence of the mutated CDH2 protein compared with wild-type CDH2 protein, which suggested that the mutated CDH2 protein's adhesion capacity was impaired. The variant was probably pathogenic after integrating clinical manifestations, genetic analysis, and functional tests. Conclusion We identified a CDH2 variant in DCM. We observed a new clinical symptom associated with N-cadherin deficiency and broadened the genetic spectra of DCM.

Identification of a novel variant in N-cadherin associated with dilated cardiomyopathy

Albinism is a group of inherited disorders mainly affecting skin, hair and eyes. Here we identify a de novo point mutation, p.R210C, in the TPCN2 gene which encodes Two Pore Channel 2 (TPC2) from a patient with albinism. TPC2 is an endolysosome and melanosome localized non-selective cation channel involved in regulating pigment production. Through inside-out recording of plasma membrane targeted TPC2 and direct recording of enlarged endolysosomal vacuoles, we reveal that the R210C mutant displays constitutive channel activation and markedly increased affinity to PI(3,5)P2. Mice harboring the homologous mutation, R194C, also exhibit hypopigmentation in the fur and skin, as well as less pigment and melanosomes in the retina in a dominant inheritance manner. Moreover, mouse embryonic fibroblasts carrying the R194C mutation show enlarged endolysosomes, enhanced lysosomal Ca2+ release and hyper-acidification. Our data suggest that R210C is a pathogenic gain-of-function TPC2 variant that underlies an unusual dominant type of albinism. 

/pdf/a-gain-of-function-tpc2-variant-r210c-increases-affinity-to-1g0j9zn5.pdf

A gain-of-function TPC2 variant R210C increases affinity to PI(3,5)P2 and causes lysosome acidification and hypopigmentation

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Affinity chromatography assisted comprehensive phosphoproteomics analysis of human saliva for lung cancer

Identification of a novel variant in N-cadherin associated with dilated cardiomyopathy

A gain-of-function TPC2 variant R210C increases affinity to PI(3,5)P2 and causes lysosome acidification and hypopigmentation