Protein tyrosine-O-sulfation in the retina

Kanan, Yogita; Hoffhines, Adam; Rauhauser, Alysha; Murray, Anne R.; Al‐Ubaidi, Muayyad R.

doi:10.1016/j.exer.2009.05.010

Cited by 18 publications

(41 citation statements)

References 36 publications

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“…We have previously shown that transcripts for both Tpst1 and Tpst2 are expressed in human and mouse retina [8]. Both transcripts are expressed in the mouse retina as early as P1, although transcript levels fluctuate over the course of retinal development [10].…”

Section: Resultsmentioning

confidence: 99%

Differential Developmental Deficits in Retinal Function in the Absence of either Protein Tyrosine Sulfotransferase-1 or -2

et al. 2012

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To investigate the role(s) of protein-tyrosine sulfation in the retina and to determine the differential role(s) of tyrosylprotein sulfotransferases (TPST) 1 and 2 in vision, retinal function and structure were examined in mice lacking TPST-1 or TPST-2. Despite the normal histologic retinal appearance in both Tpst1−/− and Tpst2−/− mice, retinal function was compromised during early development. However, Tpst1−/− retinas became electrophysiologically normal by postnatal day 90 while Tpst2−/− mice did not functionally normalize with age. Ultrastructurally, the absence of TPST-1 or TPST-2 caused minor reductions in neuronal plexus. These results demonstrate the functional importance of protein-tyrosine sulfation for proper development of the retina and suggest that the different phenotypes resulting from elimination of either TPST-1 or -2 may reflect differential expression patterns or levels of the enzymes. Furthermore, single knock-out mice of either TPST-1 or -2 did not phenocopy mice with double-knockout of both TPSTs, suggesting that the functions of the TPSTs are at least partially redundant, which points to the functional importance of these enzymes in the retina.

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Section: Resultsmentioning

confidence: 99%

Differential Developmental Deficits in Retinal Function in the Absence of either Protein Tyrosine Sulfotransferase-1 or -2

et al. 2012

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“…The sources of IPM proteins are the retina and the RPE. 6 For simplicity, henceforth the use of the abbreviation ECM covers both.…”

Section: Retinal Extracellular Matrixmentioning

confidence: 99%

A Perspective on the Role of the Extracellular Matrix in Progressive Retinal Degenerative Disorders

Al‐Ubaidi

Naash²,

Conley³

2013

Invest. Ophthalmol. Vis. Sci.

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Progressive inherited retinal degenerative disorders (PIRDDs) are the leading cause of blindness in developed countries, with AMD and RP constituting the majority of PIRDDs. Currently, over 8 million Americans have PIRDDs, and that number is estimated to drastically increase by the end of this decade. Although a mutant protein is expressed starting early during retinal development in patients with PIRDDs, symptoms of retinal degeneration do not manifest until much later. Historically, research has focused on understanding the role a mutation has in the function of a protein and what role the mutant protein has in the disease process. However, it remains unknown why the disease, irrespective of the mutation, manifests clinically much later in life, while cellular indicators of disease (e.g., accumulation of toxic protein products and cell death) occur throughout early and middle life. Herein, we propose that there exists a time point at which the degenerative process is accelerated, leading to the appearance of clinical symptoms. This point is defined by structural disruptions of the extracellular matrix (ECM). Death of a critical number of ECM-maintaining mutant protein-expressing retinal cells contributes to that break point in the degenerative process. Therefore, it is important to understand the changes occurring at the ECM during PIRDDs and to take that into account when therapeutic approaches are designed.

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“…Protein was estimated, fractionated, and transferred to membranes and immunoblotted as described previously (31).…”

Section: Methodsmentioning

confidence: 99%

“…For immunoprecipitation, 500 g of protein extracts were incubated with the desired antibody for 12 h, precipitated by centrifugation, eluted in 1ϫ Laemmli buffer (33), and fractionated by SDS-PAGE as described previously (31).…”

Section: Methodsmentioning

confidence: 99%

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Fibulin 2, a Tyrosine O-Sulfated Protein, Is Up-regulated Following Retinal Detachment

Kanan

Brobst

Han

et al. 2014

Journal of Biological Chemistry

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Protein tyrosine-O-sulfation in the retina

Cited by 18 publications

References 36 publications

Differential Developmental Deficits in Retinal Function in the Absence of either Protein Tyrosine Sulfotransferase-1 or -2

Differential Developmental Deficits in Retinal Function in the Absence of either Protein Tyrosine Sulfotransferase-1 or -2

A Perspective on the Role of the Extracellular Matrix in Progressive Retinal Degenerative Disorders

Fibulin 2, a Tyrosine O-Sulfated Protein, Is Up-regulated Following Retinal Detachment

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