Alpha-enolase

Source: Wikipedia, the free encyclopedia.

ENO1
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_001201483
NM_001428
NM_001353346

NM_023119
NM_001379127
NM_001379128

RefSeq (protein)

NP_001188412
NP_001419
NP_001340275

NP_001366056
NP_001366057
NP_075608
NP_001020559

Location (UCSC)Chr 1: 8.86 – 8.88 MbChr 4: 150.32 – 150.33 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Enolase 1 (ENO1), more commonly known as alpha-enolase, is a

Hashimoto encephalopathy.[5]

Structure

ENO1 is one of three enolase isoforms, the other two being

tumor cells.[9]

Relationship to Myc-binding protein-1

The mRNA transcript of the ENO1 gene can be alternatively translated into a

N-terminal region of the MBP1 protein it critical to DNA binding and, thus, its inhibitory function.[10]

Function

As an enolase, ENO1 is a glycolytic enzyme the catalyzes the conversion of

Clinical significance

Cancer

ENO1 overexpression has been associated with multiple tumors, including

tumorigenesis by activating plasminogen.[6][9] Moreover, ENO1 is expressed on the tumor cell surface during pathological conditions such as inflammation, autoimmunity, and malignancy. Its role as a plasminogen receptor leads to extracellular matrix degradation and cancer invasion.[9][13][14] Due to its surface expression, targeting surface ENO1 enables selective targeting of tumor cells while leaving the ENO1 inside normal cells functional.[9] Moreover, in tumors such as non-Hodgkin lymphomas (NHLs) and breast cancer, inhibition of ENO1 expression decreased tolerance to hypoxia while increasing sensitivity to radiation therapy, thus indicating that ENO1 may have aided chemoresistance.[6][11] Considering these factors, ENO1 holds great potential to serve as an effective therapeutic target for treating many types of tumors in patients.[6][11][13]

ENO1 is located on the 1p36 tumor suppressor locus near

ENO2 for the execution of glycolysis.[17][18] Tumor cells with such deletions are exceptionally sensitive towards ablation of ENO2.[17][18] Inhibition of ENO2 in ENO1-homozygously deleted cancer cells constitutes an example of synthetic lethality
treatment for cancer.

Autoimmune disease

ENO1 has been detected in serum drawn from children diagnosed with juvenile idiopathic arthritis.[19]

Alpha-enolase has been identified as an

autoantigen in Hashimoto's encephalopathy.[20] Single studies have also identified it as an autoantigen associated with severe asthma[21] and a putative target antigen of anti-endothelial cell antibody in Behçet's disease.[22] Reduced expression of the enzyme has been found in the corneal epithelium of people suffering from keratoconus.[23][24]

Gastrointestinal disease

pylori-mediated gastric diseases.[14]

Hemolytic anemia

Enolase deficiency is a rare inborn error of metabolism disease, leads to hemolytic anemia in affected homozygous carriers of loss of function mutations in ENO1.[25] As with other glycolysis enzyme deficiency diseases, the condition is aggravated by redox-cycling agents such as nitrofurantoin.

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles.[§ 1]

[[File:
GlycolysisGluconeogenesis_WP534go to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to WikiPathwaysgo to articlego to Entrezgo to article
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GlycolysisGluconeogenesis_WP534go to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to WikiPathwaysgo to articlego to Entrezgo to article
|alt=Glycolysis and Gluconeogenesis edit]]
Glycolysis and Gluconeogenesis edit
  1. ^ The interactive pathway map can be edited at WikiPathways: "GlycolysisGluconeogenesis_WP534".

Interactions

Alpha-enolase has been shown to

interact with TRAPPC2.[26]

See also

External links

References

This article incorporates text from the United States National Library of Medicine, which is in the public domain.