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Genes & Diseases

Qiang Wei, Junyi Liao, Xinyi Yu, Eric J Wang, Claire Wang, Hue H Luu, Rex C Haydon, Michael J Lee, Tong-Chuan He
While CRISPR/Cas9-mediated genome editing technology has been experiencing a rapid transformation during the past few years, a recent report on NgAgo-mediated single-stranded DNA-guided genome editing may offer an attractive alternative for genome manipulation. While it's too early to predict whether NgAgo will be able to compete with or be superior to CRISPR/Cas9, the scientific community is anxiously waiting for further optimization and broader applications of the NgAgo genome editing technology.
September 2016: Genes & Diseases
Yi Feng, Brian Egan, Jinxi Wang
Low back pain (LBP) is a major cause of disability and imposes huge economic burdens on human society worldwide. Among many factors responsible for LBP, intervertebral disc degeneration (IDD) is the most common disorder and is a target for intervention. The etiology of IDD is complex and its mechanism is still not completely understood. Many factors such as aging, spine deformities and diseases, spine injuries, and genetic factors are involved in the pathogenesis of IDD. In this review, we will focus on the recent advances in studies on the most promising and extensively examined genetic factors associated with IDD in humans...
September 2016: Genes & Diseases
Jun Sun, Ikuko Kato
Although genes contribute to colorectal cancer, the gut microbiota are an important player. Accumulating evidence suggests that chronic infection and the ensuing inflammation contributes to tumor initiation and tumor progression. A variety of bacterial species and tumor-promoting virulence mechanisms have been investigated. Significant advances have been made in understanding the composition and functional capabilities of the gut microbiota and its roles in cancer. In the current review, we discuss the novel roles of microbiota in the progression of colon cancer...
June 2016: Genes & Diseases
Baozhong Zhao, Lei Qiang, Joy Joseph, Balaraman Kalyanaraman, Benoit Viollet, Yu-Ying He
Autophagy is a cellular self-eating process essential for stress response and maintaining tissue homeostasis by lysosomal degradation of unwanted or damaged proteins and organelles. Here, we show that cells with defective mitochondria induce autophagy to promote cell survival through activating the AMPK pathway. Loss of mitochondrial complex III protein cytochrome b activates the AMPK signaling and induced autophagy. Inhibiting mitochondria energetics by mitochondria-targeted agents activates the AMPK signaling and induced autophagy...
March 2016: Genes & Diseases
Hua Geng, Xiao-Di Tan
Precise and dynamic regulation of gene expression is a key feature of immunity. In recent years, rapid advances in transcriptome profiling analysis have led to recognize long non-coding RNAs (lncRNAs) as an additional layer of gene regulation context. In the immune system, lncRNAs are found to be widely expressed in immune cells including monocytes, macrophages, dendritic cells (DCs), neutrophils, T cells and B cells during their development, differentiation and activation. However, the functional importance of immune-related lncRNAs is just emerging to be characterized...
March 2016: Genes & Diseases
Viktor Tollemar, Zach J Collier, Maryam K Mohammed, Michael J Lee, Guillermo A Ameer, Russell R Reid
Current reconstructive approaches to large craniofacial skeletal defects are often complicated and challenging. Critical-sized defects are unable to heal via natural regenerative processes and require surgical intervention, traditionally involving autologous bone (mainly in the form of nonvascularized grafts) or alloplasts. Autologous bone grafts remain the gold standard of care in spite of the associated risk of donor site morbidity. Tissue engineering approaches represent a promising alternative that would serve to facilitate bone regeneration even in large craniofacial skeletal defects...
March 2016: Genes & Diseases
Saint-Aaron L Morris, Suyun Huang
Many cancers have similar aberrations in various signaling cascades with crucial roles in cellular proliferation, differentiation, and morphogenesis. Dysregulation of signal cascades that play integral roles during early cellular development is well known to be a central feature of many malignancies. One such signaling cascade is the Wnt/β-catenin pathway, which has a profound effect on stem cell proliferation, migration, and differentiation. This pathway is dysregulated in numerous cell types, underscoring its global oncogenetic potential...
March 2016: Genes & Diseases
Maryam K Mohammed, Connie Shao, Jing Wang, Qiang Wei, Xin Wang, Zachary Collier, Shengli Tang, Hao Liu, Fugui Zhang, Jiayi Huang, Dan Guo, Minpeng Lu, Feng Liu, Jianxiang Liu, Chao Ma, Lewis L Shi, Aravind Athiviraham, Tong-Chuan He, Michael J Lee
Wnt signaling transduces evolutionarily conserved pathways which play important roles in initiating and regulating a diverse range of cellular activities, including cell proliferation, calcium homeostasis, and cell polarity. The role of Wnt signaling in control of cell proliferation and stem cell self-renewal is primarily carried out through the canonical pathway, which is the best characterized among the multiple Wnt signaling branches. The past 10 years has seen a rapid expansion in our understanding of the complexity of this pathway, as many new components of Wnt signaling have been identified and linked to signaling regulation, stem cell functions, and adult tissue homeostasis...
March 2016: Genes & Diseases
Leonid V Kapilevich, Tatyana A Kironenko, Anna N Zaharova, Yuri V Kotelevtsev, Nickolai O Dulin, Sergei N Orlov
During the last two decades numerous research teams demonstrated that skeletal muscles function as an exercise-dependent endocrine organ secreting dozens of myokines. Variety of physiological and pathophysiological implications of skeletal muscle myokines secretion has been described; however, upstream signals and sensing mechanisms underlying this phenomenon remain poorly understood. It is well documented that in skeletal muscles intensive exercise triggers dissipation of transmembrane gradient of monovalent cations caused by permanent activation of voltage-gated Na(+) and K(+) channels...
December 2015: Genes & Diseases
Fei Li, Jim Hu
No abstract text is available yet for this article.
December 1, 2015: Genes & Diseases
Sarah M Lyon, Darrel Waggoner, Sara Halbach, Erik C Thorland, Leila Khorasani, Russell R Reid
Craniosynostosis, a condition in which the cranial sutures prematurely fuse, can lead to elevated intracranial pressure and craniofacial abnormalities in young children. Currently surgical intervention is the only therapeutic option for patients with this condition. Craniosynostosis has been associated with a variety of different gene mutations and chromosome anomalies. Here we describe three cases of partial deletion of chromosome 19p. Two of the cases present with syndromic craniosynostosis while one has metopic ridging...
December 2015: Genes & Diseases
Fei Li, Jim Hu, Keping Xie, Tong-Chuan He
No abstract text is available yet for this article.
December 2015: Genes & Diseases
Jordan D Green, Viktor Tollemar, Mark Dougherty, Zhengjian Yan, Liangjun Yin, Jixing Ye, Zachary Collier, Maryam K Mohammed, Rex C Haydon, Hue H Luu, Richard Kang, Michael J Lee, Sherwin H Ho, Tong-Chuan He, Lewis L Shi, Aravind Athiviraham
Defects of articular cartilage present a unique clinical challenge due to its poor self-healing capacity and avascular nature. Current surgical treatment options do not ensure consistent regeneration of hyaline cartilage in favor of fibrous tissue. Here, we review the current understanding of the most important biological regulators of chondrogenesis and their interactions, to provide insight into potential applications for cartilage tissue engineering. These include various signaling pathways, including: fibroblast growth factors (FGFs), transforming growth factor β (TGF-β)/bone morphogenic proteins (BMPs), Wnt/β-catenin, Hedgehog, Notch, hypoxia, and angiogenic signaling pathways...
December 2015: Genes & Diseases
Connie Shao, Christine Shen, Emily Lu, Rex C Haydon, Hue H Luu, Aravind Athiviraham, Tong-Chuan He, Michael J Lee
Increasing prostaglandin E2 by knocking out its inhibitor 15-hydroxyprostaglandin dehydrogenase (15-PDGH) or administering a compound that inhibits 15-PDGH was recently found to improve healing in hematopoietic stem cell transplants, colitis recovery, and hepatogenesis after transection in mice. These results are suggestive of pharmacologic therapies or even genetic therapy that could improve patient outcomes, especially since the excess PGE2 and the 15-PDGH inhibitor have proven to be non-toxic. However, elevated levels of PGE2 are associated with increased risk of cancer and blood clotting problems...
December 2015: Genes & Diseases
Jim Hu, Tong-Chuan He, Fei Li
Vision loss or impairment resulting from the degeneration of the retinal pigment epithelium and photoreceptor death affects millions worldwide. Recent exciting results from clinical studies of small numbers of patients treated with human embryonic stem cell-derived retinal pigment epithelial cells may provide hope for affected individuals.
December 2015: Genes & Diseases
Mohamed Jamal, Sami M Chogle, Sherif M Karam, George T-J Huang
NOTCH plays a role in regulating stem cell function and fate decision. It is involved in tooth development and injury repair. Information regarding NOTCH expression in human dental root apical papilla (AP) and its residing stem cells (SCAP) is limited. Here we investigated the expression of NOTCH3, its ligand JAG1, and mesenchymal stem cell markers CD146 and STRO-1 in the AP or in the primary cultures of SCAP isolated from AP. Our in situ immunostaining showed that in the AP NOTCH3 and CD146 were co-expressed and associated with blood vessels having NOTCH3 located more peripherally...
September 2015: Genes & Diseases
Jing Wang, Qiang Wei, Jixing Ye, Sahitya K Denduluri, Xin Wang, Maryam K Mohammed, Hue H Luu, Rex C Haydon, Tong-Chuan He
Cancer death is usually caused by incurable drug-resistant and metastatic cancers. Although tremendous progress has been made in anticancer drug development during the past two decades, cancer medicine still faces unprecedented challenges associated with choosing effective treatments for individual patients. Three recent reports have offered encouraging approaches towards potentially personalized cancer drug selection.
September 2015: Genes & Diseases
Resham Bhattacharya, Soumyajit Banerjee Mustafi, Mark Street, Anindya Dey, Shailendra Kumar Dhar Dwivedi
Bmi-1 is a member of the Polycomb Repressor Complex1 that mediates gene silencing by regulating chromatin structure and is indispensable for self-renewal of both normal and cancer stem cells. Despite three decades of research that have elucidated the transcriptional regulation, post-translational modifications and functions of Bmi-1 in regulating the DNA damage response, cellular bioenergetics, and pathologies, the entire potential of a protein with such varied function remains to be realized. This review attempts to synthesize the current knowledge on Bmi-1 with an emphasis on its role in both normal physiology and cancer...
September 2015: Genes & Diseases
Matthew D Lynes, Yu-Hua Tseng
In mammals, a thermogenic mechanism exists that increases heat production and consumes energy. Recent work has shed light on the cellular and physiological mechanisms that control this thermogenic circuit. Thermogenically active adipocytes, namely brown and closely related beige adipocytes, differentiate from progenitor cells that commit to the thermogenic lineage but can arise from different cellular origins. Thermogenic differentiation shares some features with general adipogenesis, highlighting the critical role that common transcription factors may play in progenitors with divergent fates...
June 2015: Genes & Diseases
Henriette Stoy, Vsevolod V Gurevich
Activating and inactivating mutations in numerous human G protein-coupled receptors (GPCRs) are associated with a wide range of disease phenotypes. Here we use several class A GPCRs with a particularly large set of identified disease-associated mutations, many of which were biochemically characterized, along with known GPCR structures and current models of GPCR activation, to understand the molecular mechanisms yielding pathological phenotypes. Based on this mechanistic understanding we also propose different therapeutic approaches, both conventional, using small molecule ligands, and novel, involving gene therapy...
June 2015: Genes & Diseases
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