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For example, BRUNOL1 (also known as CELF3), a brain-testis specific RNA binding protein, is also expressed in the haploid stage of spermatogenesis.
The transcriptional co-activator CREB binding protein is also a target for p90 RSK [ 53].
Like transthyretin, retinol binding protein is also a negative acute phase protein and its production is inhibited by proinflammatory cytokines [ 23].
For example, the character of ASAP as a microtubule binding protein is also found with the structural domains that ASAP shares with MAP1A.
Cirp, coding for cold inducible RNA binding protein, is also upregulated by sleep in astrocytes and oligodendrocytes [ 37], and was identified as a sleep gene in previous studies that pooled transcripts from all brain cells [ 41– 41].
It is known that the poly(A) tail binding protein is also a eukaryotic translation initiation factor, which interacts with protein eIF4G of the mRNA 5′-cap structure [ 41].
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Four genes related to DNA repair, replication protein A, formamidopyrimidine-DNA glycosylase, DNA repair protein RAD51 and DNA binding protein were also up-regulated in Kavya (Additional file 4: Figure S3).
Serum vitamin D binding protein was also measured by an immuno-pelometric assay.
Hax1, another Vimentin mRNA binding protein, was also shown to be present in HeLa cell nuclear extracts.
Interestingly, mutations in Tau, a microtubule binding protein, are also extensively documented in Alzheimer's (reviewed in [51], [52]).
Similarly, Sbp, amino acid-binding periplasmic protein and putative exported solute binding protein are also identified as members of the SBP_bac_1, SBP_bac_3 and SBP_bac_7 families of bacterial extracellular solute-binding proteins, respectively, indicating their potential for secretion into the extracellular space.
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