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Singular Cells Protect Themselves from Protein Clumps

Research has been found as to how cells protect themselves from protein clumps, which are the causes of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington disease.

The University of Glasgow and The University of Dundee collaborate with the MRC Protein Phosphorylation unit to give us further information on the role of the gene UBQLN2 which is also known as the same gene that removes toxic protein clumps and protects us from diseases.

Researchers have discovered that UBQLN2 role is to straighten out clumps and iron out all tangles to ensure future prevention. The researchers made use of Biochemistry, cell biology, and cultured mouse models. This method helped them prove their theory in what steps to follow.

University of Glasgow

Neurodegenerative diseases are the outcome of UBQLN2 gene being either defective or mutates to which it will not be able to remove toxic clumps. The natural aging process plays a role in being more vulnerable to protein clumps although usually detangled and disposed of.

The purpose of UBQNL2

The UBQNL2 encoded gene has an protein similar to ubiquitin, sharing a high amount of resemblance with yeast-like products. Ubiquilins has a C-terminal ubiquitin-associated domain and an N-terminal ubiquitin-like domain. They associate with proteasomes and ubiquitin ligases and are thought to link the ubiquitination machinery functionally to the proteasome, effecting in vivo protein degradation. The ubiquilin has also revealed to bind the ATPase domain of the Hsp70-like Stch protein. The purpose of UBQNL2 is linked to numerous neurodegenerative illnesses mainly Parkinson’s, Alzheimer’s and hunting diseases. Dr. Thimo Kurz mastering System biology and cells explain the uncanny link between these cells and diseases.

An experiment was done using mice that imitate the human Hunting disease that revealed that the UBQLN2 gene had mutated and as a result could not assist nerve cells to eliminate protein clumps that formed the brains of the tested mice.


Prior to this study, there was a misunderstanding as to why the gene caused diseases. Preceding experiments and extensive research revealed that when the UBQLN2 gene is defective or faulty, it leads to Amyotrophic Lateral Sclerosis with Frontotemporal Dementia, which may also be known as ALS/FTD or Motor neuron with Dementia.
Due to these discoveries unraveling how the UBQLN2 gene works and what role it plays, scientist now has a better understanding as to why the genes mutated transformation appears so detrimental to the human body.

Patients with neurodegenerative diseases may look forward to novel treatment as unraveling the UBQLN2 gene is being researched extensively. This treatment can improve their quality of life and perhaps allow human beings to function normally.

Dr Roland Hjerpe stated that he believes the significance of the discovery needs to go beyond the role of UBQLN2 in diseases such as dementia that affects motor neuron. Any discovery that involves neuron activity is linked in some way or another so the finding of one needs to broaden to others where possible.

The study has presented a new way in which the nerve cells learn to cope with the protein clumps in a general way. This has implications for the most neurodegenerative diseases, which in turn can reveal new avenues for therapeutic interventions so that these conditions can be treated in the future.