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Cell
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August 13, 2005
Rpe65 is the retinoid isomerase in bovine retinal pigment epithelium
Minghao Jin, Songhua Li, Walid N Moghrabi, et al.
Biochimica Et Biophysica Acta. Gene Regulatory Mechanisms
|
February 8, 2018
The AU-rich element landscape across human transcriptome reveals a large proportion in introns and regulation by ELAVL1/HuR
Tala Bakheet, Edward Hitti, Maher Al-Saif, et al.
The Journal of Biological Chemistry
|
October 9, 2003
Rpe65 is a retinyl ester binding protein that presents insoluble substrate to the isomerase in retinal pigment epithelial cells
Nathan L Mata, Walid N Moghrabi, Jung S Lee, et al.
Molecular Oncology
|
January 7, 2021
Kinome inhibition reveals a role for polo-like kinase 1 in targeting post-transcriptional control in cancer
Qamraa H Al-Qahtani, Walid N Moghrabi, Suhad Al-Yahya, et al.
Genome Biology
|
July 30, 2017
A novel mechanism for variable phenotypic expressivity in Mendelian diseases uncovered by an AU-rich element (ARE)-creating mutation
Nisha Patel, Arif O Khan, Maher Al-Saif, et al.
Page
of 1
Search research articles
Search
Showing results (1-10 of 5) with videos related to
Sort By:
Page
of 1
Cell
|
August 13, 2005
Rpe65 is the retinoid isomerase in bovine retinal pigment epithelium
Minghao Jin, Songhua Li, Walid N Moghrabi, et al.
Biochimica Et Biophysica Acta. Gene Regulatory Mechanisms
|
February 8, 2018
The AU-rich element landscape across human transcriptome reveals a large proportion in introns and regulation by ELAVL1/HuR
Tala Bakheet, Edward Hitti, Maher Al-Saif, et al.
The Journal of Biological Chemistry
|
October 9, 2003
Rpe65 is a retinyl ester binding protein that presents insoluble substrate to the isomerase in retinal pigment epithelial cells
Nathan L Mata, Walid N Moghrabi, Jung S Lee, et al.
Molecular Oncology
|
January 7, 2021
Kinome inhibition reveals a role for polo-like kinase 1 in targeting post-transcriptional control in cancer
Qamraa H Al-Qahtani, Walid N Moghrabi, Suhad Al-Yahya, et al.
Genome Biology
|
July 30, 2017
A novel mechanism for variable phenotypic expressivity in Mendelian diseases uncovered by an AU-rich element (ARE)-creating mutation
Nisha Patel, Arif O Khan, Maher Al-Saif, et al.
Page
of 1