in the diabetic retinopathy environment TTR might affect the lncRNA MEG3/miR-223-3p axis by the direct binding with PABPC1 and finally repress retinal vessel proliferation.
PIWIL1 augments protein translation with PABPC1 in the presence of 3'-UTRs of post-meiotic mRNAs. While both the N-terminal RNA recognition motif (RRM) domain and the central linker region of PABPC1 stimulate translation only the PIWI Argonaute and Zwille (PAZ) domain of PIWIL1 positively affects translation of reporter mRNAs.
These results suggest that PABP interacts with HuD in basal glucose conditions making translation inhibitory complex however upon glucose stimulation this association is affected and PABP is acted upon by PDI resulting in stimulation of insulin translation.
The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase SIRT1 acts as an energy sensor and negatively regulates poly(A)RNA transport via deacetylating a poly(A)-binding protein PABP1.
The authors found that the endogenous Zfp36 directly interacts with the cytoplasmic poly(A)-binding protein. Importantly this interaction is required for the translational repression of Zfp36's target mRNAs in resolving inflammation.
Data suggest that hnRNPLL specifically associates with cytoplasmic PABPC1 in both T-lymphocytes and plasma cells; PABPC1 promotes binding of hnRNPLL to immunoglobulin H (IgH heavy chain) mRNA and regulates switching from mIgH (membrane isoform) to sIgH (secreted isoform) in plasma cells. (hnRNPLL = heterogeneous nuclear ribonucleoprotein L-like protein; PABPC1 = cytoplasmic poly[A]
These results demonstrate that EPAB is important for oocyte-somatic communication by maintaining transzonal processes and gap junctions at the preantral stage of folliculogenesis.
Data (including data from studies in knockout mice) suggest that Epab (embryonic poly(A)-binding protein) which is oocyte specific is required for ability of cumulus cells and granulosa cells to exhibit responsiveness to Egf/Egfr signaling.
our data support the concept that expanded ATXN2 undergoes progressive insolubility and affects PABPC1 by a toxic gain-of-function mechanism with tissue-specific effects which may be partially alleviated by the induction of FBXW8.
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