Corrigendum. Expression and Localization of Luman/CREB3 in Mouse Embryos during the Pre-implantation period--Genet. Mol. Res. 14 (4): 13595-13602. Published online: October 28, 2015 (DOI: 10.4238/2015.October.28.20). Corrected after publication: January 22, 2016 (DOI: 10.4238/gmr.150156091).

In regard to the affiliation mistake that was made during our correspondence in our manuscript, we write this letter in order to correct it as per my PhD requirements and this is the Final decision as I have no other option. The correction is only in the affiliation and should be: T.N. Mahmoud(1,2), P.F. Lin(1), F.L. Chen(1), J.H. Zhou(1), X.G. Wang(1), N. Wang(1), X. Li(1) and Y.P. Jin(1). (1)Key Laboratory of Animal Biotechnology of the Ministry of Agriculture, Northwest A&F University, Yangling, Shaanxi, China. (2)Department of Animal Physiology and Biochemistry, Faculty of Veterinary Medicine, Nyala University, Nyala, South Darfur, Sudan.

Expression and localization of Luman/CREB3 in mouse embryos during the pre-implantation period.

Luman/CREB3 is a transcription factor that is a member of the cAMP-response-element-binding protein family of basic region-leucine zipper transcription factors. This protein interacts with host cell factor 1, which also associates with the herpes simplex virus protein VP16 to induce the transcription of herpes simplex virus. Currently, the physiological function of Luman/CREB3 in reproductive processes remains unclear. In this study, quantitative real-time PCR and immunofluorescence assays were used to investigate the expression and localization of Luman in mouse oocytes as well as in early embryonic development. Luman protein was detected in the germinal vesicle and metaphase II stage oocytes, and was distributed in the cytoplasm, nucleus, and polar body of the oocyte stage. However, Luman protein and mRNA expression levels were significantly (P < 0.05) increased before activation of the zygotic genome, and expression levels peaked in 4-cell embryos. Expression levels were significantly (P < 0.05) decreased following the 8-cell stage throughout the blastocyst stage. The Luman protein was also distributed in the nucleus and cytoplasm in the early preimplantation embryo and showed enhanced nuclear staining starting from the 2-cell stage embryo up to the 8-cell stage embryo. The differences in the expression and localization of Luman in mouse oocytes and early embryo suggested that Luman plays an important role in oocyte maturation and early embryonic development processes.

Silencing effect of lentiviral vectors encod-ing shRNA of Herp on endoplasmic reticulum stress and inflammatory responses in RAW 264.7 macrophages.

Herp, a mammalian protein with a ubiquitin-like domain, can be strongly upregulated by endoplasmic reticulum (ER) stress during ER-associated protein degradation. However, the other cellular functions of Herp remain unclear. We explored the effect of Herp on ER stress and inflammatory responses in RAW 264.7 macrophages that had been exposed to tunicamycin or thapsigargin. We successfully constructed recombinant lentiviral vectors for Herp short-hairpin RNA (shRNA) expression to better understand the contribution made by Herp to other signaling pathways. Western blotting revealed that the recombinant Herp lentiviral shRNA vector significantly inhibited the expression of the Herp protein in the thapsigargin-treated RAW 264.7 macrophages. The reverse transcription quantitative polymerase chain reaction results showed that knockdown Herp inhibited the expression of ER stress-related genes during exposure to tunicamycin or thapsigargin. In RAW 264.7 macrophages, knockdown Herp markedly attenuated the expression of inflammatory cytokines when exposed to tunicamycin; however, it strongly enhanced the expression of inflammatory cytokines when exposed to thapsigargin. We concluded that Herp lentiviral shRNA vectors had been successfully constructed; knockdown Herp inhibited ER stress and had a different effect on inflammatory responses in RAW 264.7 macrophages depending on whether they were exposed to tunicamycin or thapsigargin.

Discovery of somatic mutations in the progression of chronic myeloid leukemia by whole-exome sequencing.

We performed whole-exome sequencing in samples representing accelerated phase (AP) and blastic crisis (BC) in a subject with chronic myeloid leukemia (CML). A total of 12.74 Gb clean data were generated, achieving a mean depth coverage of 64.45 and 69.53 for AP and BC samples, respectively, of the target region. A total of 148 somatic variants were detected, including 76 insertions and deletions (indels), 64 single-nucleotide variations (SNV), and 8 structural variations (SV). On the basis of annotation and functional prediction analysis, we identified 3 SNVs and 6 SVs that showed a potential association with CML progression. Among the genes that harbor the identified variants, GATA2 has previously been reported to play important roles in the progression from AP to BC in CML. Identification of these genes will allow us to gain a better understanding of the pathological mechanism of CML and represents a critical advance toward new molecular diagnostic tests for the development of potential therapies for CML.