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Expression of Syk in non-small cell lung cancer and its relationship with clinicopathological parameters

Fen LAN, Shengdao XIONG, Weining XIONG, Guopeng XU, Xiaoxia LU

《医学前沿（英文）》 2009年 第3卷 第1期   页码 41-44 doi: 10.1007/s11684-009-0009-6

摘要： This study aims to research the expression of spleen tyrosine kinase (Syk) in non-small cell lung cancer (NSCLC) and the relationship between Syk and clinicopathologic factors and p53. Immunohistochemistry was applied to detect the expression of Syk and p53 protein in 39 cases of NSCLC (23 cases of lung squamous cell cancer, 16 cases of lung adenocarcinoma) and tumor-surrounding normal lung tissues. The positive rate of Syk was 46.15% (18/39) and 100% (39/39) in NSCLC and tumor-surrounding normal lung tissues, respectively. The expression level of Syk in NSCLC was significantly lower than that in tumor-surrounding normal lung tissues ( = 0.000). The Syk expression was positively correlated withthe p53 expression in NSCLC specimens ( = 0.025). There was no significant association between Syk expression and lymph node metastasis, differentiation degree, tumor size and tumor node metastasis (TNM). The present study demonstrated that Syk was aberrantly expressed in the NSCLC and might have a significant impact on tumor growth and progression.

关键词： Syk kinase     carcinoma     non-small-cell lung     tumor suppressor protein p53    

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p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell

Junfang JI, Kun WU, Min WU, Qimin ZHAN,

《医学前沿（英文）》 2010年 第4卷 第4期   页码 412-418 doi: 10.1007/s11684-010-0260-x

摘要： mutations have been found in many esophageal squamous cell carcinoma (ESCC) clinical specimens and cell lines. We reasoned that functional inactivation of wild-type or the functional activation of mutant-type might exist in these specimens and cell lines. In this study, we identified the correlation between p53 functional activation and its genotype in five different ESCC cell lines. To examine the potential p53 activation in a certain ESCC cell line, DNA damage methods including X-ray exposure and cisplatin treatment were employed to treat cells. Further, the expression of p53 protein and four transcripts of well-known p53 target genes were investigated using Western blot and reverse transcription-polymerase chain reaction (RT-PCR) after cell exposure to DNA damage. The results showed that in KYSE 30 cell line with mutant and KYSE 150 with wild-type , p53 could be activated by DNA damages. However, p53 could not be activated following the DNA damages in YES 2 with wild-type , KYSE 70 with mutant , and EC9706 with unknown genotype. All our data indicated that p53 function in certain cells is not closely correlated with its genotype. To judge p53 function in a particular cell line, it is important to examine the p53 functional activation, but not to simply rely on the genotype.

关键词： p53     esophageal squamous cell carcinoma     DNA damage    

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Discovery and development of synthetic tricyclic pyrroloquinone (TPQ) alkaloid analogs for human cancer therapy

Wei Wang,Bhavitavya Nijampatnam,Sadanandan E. Velu,Ruiwen Zhang

《化学科学与工程前沿（英文）》 2016年 第10卷 第1期   页码 1-15 doi: 10.1007/s11705-016-1562-6

摘要： Natural products and their derivatives represent a rich source for the discovery and development of new cancer therapeutic drugs. Bioactive components derived from natural sources including marine compounds have been shown to be effective agents in the clinic or in preclinical settings. In the present review, we present a story of discovery, synthesis and evaluation of three synthetic tricyclic pyrroloquinone (TPQ) alkaloid analogs as cancer therapeutic agents. Chemical synthesis of these compounds (BA-TPQ, TBA-TPQ, and TCBA-TPQ) has been accomplished and the mechanisms of action (MOA) and structure-activity relationships (SAR) have been investigated. In the past, the complexity of chemical synthesis and the lack of well-defined MOA have dampened the enthusiasm for the development of some makaluvamines. Recent discovery of novel molecular targets for these alkaloids (unrelated to inhibition of Topoisomerase II) warrant further consideration as clinical candidates in the future. In addition to the establishment of novel synthetic approaches and demonstration of and anticancer activities, we have successfully demonstrated that these makaluvamines attack several key molecular targets, including the MDM2-p53 pathway, providing ample opportunities of modulating the compound structure based on SAR and the use of such compounds in combination therapy in the future.

关键词： synthesis     marine drugs     tricyclic pyrroloquinone alkaloid     cancer therapy     MDM2     p53    

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Decitabine induces -mediated immune responses in p53-mutated triple-negative breast cancer: a clinical

《医学前沿（英文）》 doi: 10.1007/s11684-023-1016-8

摘要： p53 is mutated in half of cancer cases. However, no p53-targeting drugs have been approved. Here, we reposition decitabine for triple-negative breast cancer (TNBC), a subtype with frequent p53 mutations and extremely poor prognosis. In a retrospective study on tissue microarrays with 132 TNBC cases, DNMT1 overexpression was associated with p53 mutations (P = 0.037) and poor overall survival (OS) (P = 0.010). In a prospective DEciTabinE and Carboplatin in TNBC (DETECT) trial (NCT03295552), decitabine with carboplatin produced an objective response rate (ORR) of 42% in 12 patients with stage IV TNBC. Among the 9 trialed patients with available TP53 sequencing results, the 6 patients with p53 mutations had higher ORR (3/6 vs. 0/3) and better OS (16.0 vs. 4.0 months) than the patients with wild-type p53. In a mechanistic study, isogenic TNBC cell lines harboring DETECT-derived p53 mutations exhibited higher DNMT1 expression and decitabine sensitivity than the cell line with wild-type p53. In the DETECT trial, decitabine induced strong immune responses featuring the striking upregulation of the innate immune player IRF7 in the p53-mutated TNBC cell line (upregulation by 16-fold) and the most responsive patient with TNBC. Our integrative studies reveal the potential of repurposing decitabine for the treatment of p53-mutated TNBC and suggest IRF7 as a potential biomarker for decitabine-based treatments.

关键词： p53 mutation     triple-negative breast cancer     decitabine     DNMT1     IRF7     innate immune response    

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Correlativity study between expression of DNA double-strand break repair protein and radiosensitivityof tumor cells

Liang ZHUANG, Shiying YU, Xiaoyuan HUANG, Yang CAO, Huihua XIONG

《医学前沿（英文）》 2009年 第3卷 第1期   页码 26-29 doi: 10.1007/s11684-009-0008-7

摘要： DNA double-strand break (DSB) is generally regarded as the most lethal of all DNA lesions after radiation. Ku80, DNA-PK catalytic subunit (DNA-PKcs) and ataxia telangiectasia mutated (ATM) proteins are major DSB repair proteins. In this study, survival fraction at 2Gy (SF2) values of eight human tumor cell lines (including four human cervical carcinoma cell lines HeLa, SiHa, C33A, Caski, three human breast carcinoma cell lines MCF-7, MDA-MB-231, MDA-MB-453, and one human lung carcinoma cell line A549) were acquired by clone formation assay, and western blot was applied to detect the expressions of Ku80, DNA-PKcs and ATM protein. The correlativity of protein expression with SF2 value was analyzed by Pearson linear correlation analysis. We found that the expression of same protein in different cell lines and the expression of three proteins in the same cell line had a significant difference. The SF2 values were also different in eight tumor cell lines and there was a positive correlativity between the expression of DNA-PKcs and SF2 ( ＝0.723, = 0.043), but Ku80 and ATM expression had no correlation with SF2 ( >0.05). These findings suggest that the expression level of DNA-PKcs protein can be an indicator for predicting the radiosensitivity of tumor cells.

关键词： Ku80     DNA-PK(cs)-binding protein     human     ataxia telangiectasia mutated protein     tumor cell lines     radiosensitivity    

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Paradoxical role of Id proteins in regulating tumorigenic potential of lymphoid cells

null

《医学前沿（英文）》 2018年 第12卷 第4期   页码 374-386 doi: 10.1007/s11684-018-0652-x

摘要：

A family of transcription factors known as Id proteins, or inhibitor of DNA binding and differentiation, is capable of regulating cell proliferation, survival and differentiation, and is often upregulated in multiple types of tumors. Due to their ability to promote self-renewal, Id proteins have been considered as oncogenes, and potential therapeutic targets in cancer models. On the contrary, certain Id proteins are reported to act as tumor suppressors in the development of Burkitt’s lymphoma in humans, and hepatosplenic and innate-like T cell lymphomas in mice. The contexts and mechanisms by which Id proteins can serve in such contradictory roles to determine tumor outcomes are still not well understood. In this review, we explore the roles of Id proteins in lymphocyte development and tumorigenesis, particularly with respect to inhibition of their canonical DNA binding partners known as E proteins. Transcriptional regulation by E proteins, and their antagonism by Id proteins, act as gatekeepers to ensure appropriate lymphocyte development at key checkpoints. We re-examine the derailment of these regulatory mechanisms in lymphocytes that facilitate tumor development. These mechanistic insights can allow better appreciation of the context-dependent roles of Id proteins in cancers and improve considerations for therapy.

关键词： Id proteins     lymphoma     leukemia     T cells     B cells     tumor suppressor     oncogene    

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ECRG4: a new potential target in precision medicine

Xin Qin, Ping Zhang

《医学前沿（英文）》 2019年 第13卷 第5期   页码 540-546 doi: 10.1007/s11684-018-0637-9

摘要： Given the rapid development in precision medicine, tremendous efforts have been devoted to discovering new biomarkers for disease diagnosis and treatment. Esophageal cancer-related gene-4 ( ), which is initially known as a new candidate tumor suppressor gene, is emerging as a sentinel molecule for gauging tissue homeostasis. ECRG4 is unique in its cytokine-like functional pattern and epigenetically-regulated gene expression pattern. The gene can be released from the cell membrane upon activation and detected in liquid biopsy, thus offering considerable potential in precision medicine. This review provides an updated summary on the biology of ECRG4, with emphasis on its important roles in cancer diagnosis and therapy. The future perspectives of ECRG4 as a potential molecular marker in precision medicine are also discussed in detail.

关键词： ECRG4     tumor suppressor gene     sentinel molecule     precision medicine     cell senescence     epithelium homeostasis    

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Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cell

Hong-Zhu LU MD, Dan LIU BM, Qi-Hong FAN BM, Jian-Hua ZHOU MD,

《医学前沿（英文）》 2010年 第4卷 第1期   页码 106-111 doi: 10.1007/s11684-010-0004-y

摘要： Hepatitis B virus X protein (HBx), a 17-kd protein encoded by X gene of hepatitis B virus (HBV), has been shown to function as a transcriptional trans-activator of a variety of viral and cellular promoter/enhancer elements. The aim of the study is to investigate the extracellular regulated protein kinases (ERKs) pathway of HBx on glomerular mesangial cell (GMC) proliferation and tumor necrosis factor-α (TNF-α) expression. The HBV X gene was amplified by polymerase chain reaction (PCR), inserted into the eukaryotic expression vector pCI-neo and confirmed by restriction endonuclease digestion and sequence analysis. PCI-neo containing HBV X gene (pCI-neo-X) was then transfected into cultured GMC line via liposome. GMC proliferation, TNF-α and its mRNA expression were compared in the condition of with or without U0126 in culture media. HBx, ERK and p-ERK expression in GMCs was assessed by Western blotting. TNF-α mRNA expression was assessed by semi-quantitative reverse transcription-PCR (RT-PCR). TNF-α level in supernatants was measured by ELISA. GMC proliferation was detected by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) kit. The results showed that HBx expression was found in transfected GMCs and became prominent at 36th and 48th h after transfection whether with or without U0126 in culture media. TNF-α mRNA expression was significantly decreased in U0126 group compared with U0126-free group. TNF-α levels in supernatants in PCI-neo-X transfection without U0126 group were (189.0±18.1) and (172.3±24.3) pg/mL at 36th and 48th h after transfection, respectively. In contrast, TNF-α levels in supernatants with U0126 were (65.6±11.6) and (84.0±24.6) pg/mL at 36th and 48th h, respectively. The TNF-α levels in the latter groups were significantly lower than those in the former groups (<0.05). GMCs proliferation was also lower in added U0126 group at 36th and 48th h after transfection. From above, we can conclude that HBx could induce GMC proliferation and increase TNF-α mRNA expression and its protein production. HBx upregulates TNF-α expression and induces cell proliferation of GMC line partly through ERK signal transduction pathway.

关键词： hepatitis B virus     X gene     glomerular mesangial cell line     extracellular regulated protein kinases     tumor necrosis factor-α    

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Detecting genetic hypermutability of gastrointestinal tumor by using a forensic STR kit

Anqi Chen, Suhua Zhang, Jixi Li, Chaoneng Ji, Jinzhong Chen, Chengtao Li

《医学前沿（英文）》 2020年 第14卷 第1期   页码 101-111 doi: 10.1007/s11684-019-0698-4

摘要： Growing evidence suggests that somatic hypermutational status and programmed cell death-1 overexpression are potential predictive biomarkers indicating treatment benefits from immunotherapy using immune checkpoint inhibitors. However, biomarker-matched trials are still limited, and many of the genomic alterations remain difficult to target. To isolate the potential somatic hypermutational tumor from microsatellite instability low/microsatellite stability (MSI-L/MSS) cases, we employed two commercial kits to determine MSI and forensic short tandem repeat (STR) alternations in 250 gastrointestinal (GI) tumors. Three types of forensic STR alternations, namely, allelic loss, Aadd, and Anew, were identified. 62.4% (156/250) of the patients with GI exhibited STR alternation, including 100% (15/15) and 60% (141/235) of the microsatellite high instability and MSI-L/MSS cases, respectively. 30% (75/250) of the patients exhibited STR instability with more than 26.32% (26.32%–84.21%) STR alternation. The cutoff with 26.32% of the STR alternations covered all 15 MSI cases and suggested that it might be a potential threshold. Given the similar mechanism of the mutations of MSI and forensic STR, the widely used forensic identifier STR kit might provide potential usage for identifying hypermutational status in GI cancers.

关键词： mismatch repair protein deficiency (MMR-D)     microsatellite instability (MSI)     short tandem repeats (STR)     gastrointestinal tumor     hypermutability    

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Potential functions of esophageal cancer-related gene-4 in the cardiovascular system

Rui Zhou, Yuanshu Liu, Wenjun Huang, Xitong Dang

《医学前沿（英文）》 2019年 第13卷 第6期   页码 639-645 doi: 10.1007/s11684-019-0701-0

摘要： Esophageal cancer-related gene-4 ( ) is cloned from the normal epithelium of the esophagus. It is constitutively expressed in quiescent epithelial cells and downregulated during tumorigenesis, and expression levels are inversely correlated with the malignant phenotype of tumor cells, validating that is a real tumor suppressor gene. Unlike other tumor suppressor genes that usually encode membrane or intracellular proteins, encodes a 148-amino acid pre-pro-peptide that is tethered on the cell surface in epithelial cells, specialized epithelial cells, and human leukocytes, where it can be processed tissue dependently into several small peptides upon cell activation. Ecrg4 is expressed in a wide variety of other cells/tissues, including cardiomyocytes and conduction system of the heart，, the glomus cells of the carotid body, adrenal glands, choroid plexus, and leukocytes among others, where it exerts distinct functions, such as promoting/suppressing inflammation, inducing neuron senescence, stimulating the hypothalamus–pituitary–adrenal axis, maintaining the stemness of stem cells, participating in the rhythm and rate control of the heart, and possibly gauging the responsiveness of the cardiovascular system (CVS) to hypoxia, in addition to tumor suppression. Here, we briefly review the latest discoveries on Ecrg4 and its underlying molecular mechanisms as a tumor suppressor and focus on the emerging roles of Ecrg4 in the CVS.

关键词： tumor suppressor gene     esophageal cancer-related gene-4     cardiovascular disease     hypoxia    

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Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

《医学前沿（英文）》 2007年 第1卷 第3期   页码 248-252 doi: 10.1007/s11684-007-0047-x

摘要： The aim of this study was to investigate the role of p38 mitogen-activated protein kinase (MAPK) in cell migration induced by platelet-derived growth factor (PDGF). Western blot was performed to detect the phosphorylation of p38 in NIH3T3 cells treated with PDGF. A Transwell cell migration system was used to determine the effects of PDGF treatment on the migration of NIH3T3 cells and the influence of deficiency on this process in a gene knockout (p38) mouse embryonic fibroblast cell line. On the stimulation of PDGF, the migration of NIH3T3 cells was significantly increased (〈0.001) compared to the control and p38 MAP kinase was simultaneously phosphorylated. Furthermore, the PDGF-induced cell migration was significantly blocked in gene knockout (p38) mouse embryonic fibroblasts (MEFs) (〈0.001) as compared with the wild type cells (p38). p38 MAPK plays an important role in the regulation of cell migration induced by PDGF.

关键词： control     stimulation     mitogen-activated     growth factor     process    

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Mechanisms of connective tissue formation and blocks of mitogen activated protein kinase

Irina A SHURYGINA, Michael G SHURYGIN, Nataliya I AYUSHINOVA, Galina B GRANINA, Nikolay V ZELENIN

《化学科学与工程前沿（英文）》 2012年 第6卷 第2期   页码 232-237 doi: 10.1007/s11705-012-1286-1

摘要： Ninety male Wistar rats were selected under the “Guide for the Care and Use of Laboratory Animals” for skin-muscle wound models. Three groups of animals were examined respectively for inoculation of inhibitor of p38 MAPK (mitogen activated protein kinase) SB 203580 and JNK inhibitor SP 600125, and a control. Light microscopy, immunohistochemistry, and tensometry revealed that the inhibition of p38 or JNK cascades have modified the formation of the connective tissue scar. The degree of connective tissue growth in the area of surgical wound had been significantly reduced by the end of observation (30 d) as the SB 203580 was applied (% volume of collagen 43.60 (41.05 – 60.15) 73.54 (66.87 – 78.01) in control, = 0.002). Conversely, when we have applied the JNK blocker, the density of collagen in scar tissue increased (78.14 (72.77 – 81.14), = 0.022 control). SB203580 inhibits the expression of p38, c-Jun and c-Fos. When we have used the JNK blocker, the expression of c-Fos and c-Jun decreased, but the expression of p38 increased. This determines the high functional activity of fibroblasts after using SP 600125. Obtained results show the importance of studying regulators of cell differentiation as potential drugs, which significantly affect the outcome of the pathological processes.

关键词： connective tissue     mitogen activated protein kinase (MAPK)     p38     JNK    

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Protein phosphatase magnesium-dependent 1δ is a novel tumor marker and target in hepatocellular carcinoma

null

《医学前沿（英文）》 2016年 第10卷 第1期   页码 52-60 doi: 10.1007/s11684-016-0433-3

摘要：

Hepatocellular carcinoma (HCC) is a lethal liver malignancy worldwide. In this study, we reported that protein phosphatase magnesium-dependent 1δ (PPM1D) was highly expressed in the majority of HCC cases (approximately 59%) and significantly associated with high serum α-fetoprotein (AFP) level (P= 0.044). Kaplan-Meier and Cox regression data indicated that PPM1D overexpression was an independent predictor of HCC-specific overall survival (HR, 2.799; 95% CI, 1.346–5.818, P = 0.006). Overexpressing PPM1D promoted cell viability and invasion, whereas RNA interference-mediated knockdown of PPM1D inhibited proliferation, invasion, and migration of cultured HCC cells. In addition, PPM1D suppression by small interfering RNA decreased the tumorigenicity of HCC cells in vivo. Overall, results suggest that PPM1D is a potential prognostic marker and therapeutic target for HCC.

关键词： PPM1D     hepatocellular carcinoma     prognosis     target therapy    

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A systematic survey of LU domain-containing proteins reveals a novel human gene, LY6A, which encodes the candidate ortholog of mouse Ly-6A/Sca-1 and is aberrantly expressed in pituitary tumors

《医学前沿（英文）》 2023年 第17卷 第3期   页码 458-475 doi: 10.1007/s11684-022-0968-4

摘要： The Ly-6 and uPAR (LU) domain-containing proteins represent a large family of cell-surface markers. In particular, mouse Ly-6A/Sca-1 is a widely used marker for various stem cells; however, its human ortholog is missing. In this study, based on a systematic survey and comparative genomic study of mouse and human LU domain-containing proteins, we identified a previously unannotated human gene encoding the candidate ortholog of mouse Ly-6A/Sca-1. This gene, hereby named LY6A, reversely overlaps with a lncRNA gene in the majority of exonic sequences. We found that LY6A is aberrantly expressed in pituitary tumors, but not in normal pituitary tissues, and may contribute to tumorigenesis. Similar to mouse Ly-6A/Sca-1, human LY6A is also upregulated by interferon, suggesting a conserved transcriptional regulatory mechanism between humans and mice. We cloned the full-length LY6A cDNA, whose encoded protein sequence, domain architecture, and exon‒intron structures are all well conserved with mouse Ly-6A/Sca-1. Ectopic expression of the LY6A protein in cells demonstrates that it acts the same as mouse Ly-6A/Sca-1 in their processing and glycosylphosphatidylinositol anchoring to the cell membrane. Collectively, these studies unveil a novel human gene encoding a candidate biomarker and provide an interesting model gene for studying gene regulatory and evolutionary mechanisms.

关键词： LU domain-containing protein family     novel human gene     LY6A     pituitary tumor     biomarker     nonsynonymous SNP     GPI-anchored protein    

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Molecular characterization of two suppressor of cytokine signaling 1 genes (

Xue XU,Jiannan ZHANG,Juan LI,Yajun WANG

《农业科学与工程前沿（英文）》 2015年 第2卷 第1期   页码 73-83 doi: 10.15302/J-FASE-2015044

摘要： Suppressor of cytokine signaling 1 (SOCS1) protein can inhibit the signal transduction triggered by some cytokines or hormones and thus are important in many physiological/pathological processes, including innate and adaptive immunity, inflammation, and development in mammals. However, there is sparse information about their structure, tissue expression, in birds, where their biological functions remain unknown. In this study, we cloned and characterized two genes (named and ) from chickens. is predicted to encode a 207-amino acid protein, which shares high amino acid sequence identity (64%–67%) with human and mouse SOCS1. Besides , a novel gene was also identified in chickens and other non-mammalian vertebrates including . Chicken is predicted to encode a 212-amino acid protein, which shares only 30%–32% amino acid sequence identity with human SOCS1 and cSOCS1a. RT-PCR assay revealed that both and are widely expressed in all chicken tissues. Using a luciferase reporter assay system, we further demonstrated that transient expression of and can significantly inhibit chicken growth hormone (GH)- or prolactin (PRL)-induced luciferase activities of Hep G2 cells expressing cGH receptor (or cPRL receptor), indicating that SOCS1a and SOCS1b proteins can negatively regulate GH/PRL signaling. Taken together, these data suggest that both cSOCS1a and cSOCS1b may function as negative regulators of cytokine/hormone actions, such as modulation of GH/PRL actions in chickens.

关键词： chicken     SOCS1a     SOCS1b     growth hormone     prolactin    

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标题 作者 时间 类型 操作

Expression of Syk in non-small cell lung cancer and its relationship with clinicopathological parameters

Fen LAN, Shengdao XIONG, Weining XIONG, Guopeng XU, Xiaoxia LU

期刊论文

p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell

Junfang JI, Kun WU, Min WU, Qimin ZHAN,

期刊论文

Discovery and development of synthetic tricyclic pyrroloquinone (TPQ) alkaloid analogs for human cancer therapy

Wei Wang,Bhavitavya Nijampatnam,Sadanandan E. Velu,Ruiwen Zhang

期刊论文

Decitabine induces -mediated immune responses in p53-mutated triple-negative breast cancer: a clinical

期刊论文

Correlativity study between expression of DNA double-strand break repair protein and radiosensitivityof tumor cells

Liang ZHUANG, Shiying YU, Xiaoyuan HUANG, Yang CAO, Huihua XIONG

期刊论文

Paradoxical role of Id proteins in regulating tumorigenic potential of lymphoid cells

null

期刊论文

ECRG4: a new potential target in precision medicine

Xin Qin, Ping Zhang

期刊论文

Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cell

Hong-Zhu LU MD, Dan LIU BM, Qi-Hong FAN BM, Jian-Hua ZHOU MD,

期刊论文

Detecting genetic hypermutability of gastrointestinal tumor by using a forensic STR kit

Anqi Chen, Suhua Zhang, Jixi Li, Chaoneng Ji, Jinzhong Chen, Chengtao Li

期刊论文

Potential functions of esophageal cancer-related gene-4 in the cardiovascular system

Rui Zhou, Yuanshu Liu, Wenjun Huang, Xitong Dang

期刊论文

Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

期刊论文

Mechanisms of connective tissue formation and blocks of mitogen activated protein kinase

Irina A SHURYGINA, Michael G SHURYGIN, Nataliya I AYUSHINOVA, Galina B GRANINA, Nikolay V ZELENIN

期刊论文

Protein phosphatase magnesium-dependent 1δ is a novel tumor marker and target in hepatocellular carcinoma

null

期刊论文

A systematic survey of LU domain-containing proteins reveals a novel human gene, LY6A, which encodes the candidate ortholog of mouse Ly-6A/Sca-1 and is aberrantly expressed in pituitary tumors

期刊论文

Molecular characterization of two suppressor of cytokine signaling 1 genes (

Xue XU,Jiannan ZHANG,Juan LI,Yajun WANG

期刊论文