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A role of heterogeneous nuclear ribonucleoprotein A/Bs in telomere maintenance
Author(s) -
Wang TzuChien V,
Huang PeiRong
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.546.1
Subject(s) - telomere , heterogeneous nuclear ribonucleoprotein , heterogeneous ribonucleoprotein particle , ribonucleoprotein , telomere binding protein , gene knockdown , biology , microbiology and biotechnology , telomerase , cell growth , population , genetics , dna , rna , cell culture , dna binding protein , gene , transcription factor , medicine , environmental health
Several members of the heterogeneous nuclear ribonucleoproteins (hnRNPs) family are thought to play roles in telomere maintenance because they are known to bind to telomeric DNA and to TERRA RNA, which is now identified as an integral component of telomeric heterochromatin. We have previously shown that the members of hnRNP A/B family are the most abundant proteins in the nuclear extracts that bound specifically to G‐strand telomeric DNA. To address if members of hnRNP A/B family are essential components of a functional telomere (i.e., does hnRNP A/Bs play a structural role) or are involved in telomere length regulation, we investigated the biological effects of knocking‐down hnRNP A1, A2/B1 or A3 in OEC‐M1 cells. Transient depletion of single hnRNP A1, A2/B1 or A3 did not affect cell growth. Stable clones that were singly knock‐down for hnRNP A1, A2 or A3 displayed normal cell proliferation and their telomere lengths were stable over 100 population doublings. Interestingly, while double‐knockdown of hnRNP A1&A3 produced a moderate inhibition of cell growth, double‐knockdown of hnRNP A1&A2 completely inhibited cell growth and was accompanied with the induction of apoptosis. These results suggest that there is a functional overlap among hnRNP A1, A2, and A3. Works are in progress to determine whether the anti‐proliferation effects of double‐depleting hnRNP A/Bs may result from telomere dysfunction.