Letter to Editor: 雌性GK糖尿病大鼠的核糖，AGEs和转酮酶变化

<正>Dear Editor,Type 2 diabetes is a chronic disease characterized by high glucose levels in the blood. Recently, it has been found that type 2 diabetic patients suffer from glucose and ribose dysmetabolism[1-3]. The GotoKakizaki (GK) rat is a nonobese, nonhypertensive model of type 2 diabetes, which, like humans, shares a susceptibility locus on chromosome 10[4-5].     

链脲霉素诱导2型糖尿病雄性大鼠核糖与核糖激酶的变化（英文）

<正>Dear Editor,Type 2 diabetes mellitus (T2DM) is a metabolic disorder that impacts multiple organs including brain activity through mechanisms such as glucose toxicity,insulin resistance,mitochondrial dysfunction,and vascular damage^[1-2].As described by Su and his colleagues^[3]in 2013,type 2 diabetics had abnormally high levels of urine ribose,suggesting that the patients suffered from not only glucose metabolism disorders,but also ribose metabolism disorders^[4]...     

韩国青羊分布的变化

Amur goral(Nemorhaedus caudatus)is a rare species among Asian mammals. It is listed as Vulnerable in the 1996 IUCN Red List of the Threatened Animals[1], and designated as the natural monument (No. 217) in Republic of Korea[2]. This species is distributed in Northeast and Southwest of China, south of the Russian Far East and the Korean peninsula[3-5].But subspecies are different with inhabitants in China, which occur 5 species of gorals[4].     

Assessment and comparison of recombinant proteins from different sources for the detection of SARS-CoV-2 infection by using protein microarray

COVID-19 (the COVID-19 is a type of disease and resulted from being infected by virus SARS-CoV-2) pandemic is threatening tens of millions of lives around the world [1]. To date, specific drugs or vaccines are still not available for fighting the SARS-CoV-2. Diagnosis and quarantine are still the effective strategies for preventing the virus from spreading. Up to now, various detection methods for SARS-CoV-2 have been developed [2], which play critical roles in controlling the pandemics. According to the targets to be detected, these methods can be divided into three classes: methods for the nucleic acid [3], antigens [4], and antibodies elicited by the virus in the host [5]. Among these methods, the ones for antigens and antibodies could produce results in 10–15 min [6], which are suitable for point-of-care diagnosis, especially the ones for antibodies [7]. Meanwhile, the asymptomatic cases [8] and the false-negative results of nucleic acid testing [9] make the detection methods based on antibodies the best alternatives. The proteins, used in methods for detection of antibodies elicited by SARS-CoV-2 in the host, are critical agents, which could affect the diagnosis results. Given the strong immunogenicity of the nucleocapsid (N protein), spike protein (S protein), and related domains [10] and the potential diagnosis values, we collected 9 S1 proteins, 3 N proteins, 5 S2-related proteins, and receptor-binding domains (RBDs) from ACROBiosystems (Beijing, China), ABclonal (Wuhan, China), Novoprotein (Shanghai, China), Sino Biological (Beijing, China), and KactusBiosystems (Shanghai, China) and fabricated a protein microarray (Fig. 1A) to assess their diagnosis performance. In addition, other proteins such as the angiotensin converting enzyme 2 (ACE2), envelop protein (E), 3C-like protease, and papain-like protease were also included (Fig. 1B).     

More or less is fine: an undercover work of DKK1 in anthrax toxin uptake

<正>The protective antigen(PA)mediated internalization of the anthrax complexes is critical in the development of anthrax,which depends on specific membrane receptors,namely ANTXR1(also known as TEM8)and ANTXR2(also known as CMG2)[1].In a screen for host proteins required for anthrax toxin action,low-density lipoprotein receptor-related protein 6(LRP6)was found important for efficient toxin entry in human M2182 prostate carcinoma cells[2],which interacts with both ANTXR1 and ANTXR2.However,the role of LRP6 in anthrax toxicity remains controversial as both in mice and in human HeLa cells,knockout or knockdown of LRP6 has no clear effect on their sensitivity to anthrax toxins[3].     

Shp2, a novel oncogenic tyrosine phosphatase and potential therapeutic target for human leukemia

Shp2, encoded by the PTPNll gene in human, is a ubiquitously expressed protein tyrosine phosphatase that contains two N-terminal Src homology 2 （SH2） domains （N-SH2, C-SH2, respectively）, a catalytic protein-tyrosine phosphatase （PTP） domain, and a C-terminal tail with tyrosyl phosphorylation sites and a prolyl-rich motif [1]. The progress of our understanding of biological functions of Shp2 has clearly shown that Shp2 plays an important role not only in biology of normal hematopoietic cells and other mammalian cells, but also in the development of leukemia and other tumors. Most recently, PTPNll gene has been firmly established as the first proto-oncogene that encodes a protein tyrosine phosphatase [1-3]. In the hematopoietic system, most if not all function of Shp2 is to act as a positive component that is essential for proliferation and/or survival of hematopoietic cells through regulation of signaling pathways involving Erk, Akt and STATS [ 1-4]. Over the past few years, a number of disease-associated Shp2 mutants have been identified in human leukemia and other malignancies [1, 3, 4]. Recently, studies from our laboratories and others strongly suggest that dysregulation of wild-type Shp2 enzyme may be involved in the pathogenesis of adult leukemia [4-7]. These findings not only provide new insights into the role of Shp2 in leukemogenesis and other tumors, but also suggest new therapeutic targets for anti-leukemia drugs.     

Autoimmune Diseases in the Bioinformatics Paradigm

<正>Autoimmune diseases(AIDs)consist of a group of physiological disorders with highly diversified pathogenesis and clinical manifestations[1],which affect more than 5%of the population worldwide[2].So far,the etiology of the AIDs is still poorly understood,whereas it is generally believed that autoimmune disorder results from a complex interaction of genetic and epigenetic variations,as well as triggering environmental factors[3].Because of the varied phenotypes in different individuals of one AID and sometimes shared     

Axin bridges Daxx to p53

The death domain-associated protein Daxx exerts many reported functions that include mediating the signaling from FasL to apoptosis via activating the c-Jun N-terminal kinase （JNK） [1], induction and inhibition of apoptosis [2-5], and regulation of chromatin remodeling. It was originally cloned from a yeast two-hybrid screen using the intracellular tail of the Fas receptor as the bait [1]. Whereas many of the initial reports remain controversial, it is clear that Daxx plays important roles in the regulation of apoptosis triggered by a series of stress signals including UV irradiation, hydrogen peroxide treatment and TGF-β treatment [2, 3]. In this Commentary, we focus on Axin being a tethering factor linking Daxx to p53.