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Vascular endothelial growth factor (VEGF)-driven actin-based motility is mediated by VEGFR2 and requires concerted activation of stress-activated protein kinase 2 (SAPK2/p38) and geldanamycin-sensitive phosphorylation of focal adhesion kinase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第14期275卷 10661-10672页

作者： Rousseau, S Houle, F Kotanides, H Witte, L Waltenberger, J Landry, J Huot, J Univ Laval Hotel Dieu Quebec Ctr Rech Cancerol Quebec City PQ G1R 2J6 Canada Univ Ulm Med Ctr Dept Internal Med 2 D-89081 Ulm Germany ImClone Syst Inc Dept Mol & Cell Biol New York NY 10014 USA

In endothelial cells, vascular endothelial growth factor (VEGF) induces an accumulation of stress fibers associated with new actin polymerization and rapid formation of focal adhesions at the ventral surface of the cells. This cytoskeletal reorganization results in an intense motogenic activity. Using porcine endothelial cells expressing one or the other type of the VEGF receptors, VEGFR1 or VEGFR2, or human umbilical vein endothelial cells pretreated with a VEGFR2 neutralizing antibody, we show that VEGFR2 is responsible for VEGF-induced activation of the stress-activated protein kinase-2/p38 (SAPK2/p38), phosphorylation of focal adhesion kinase (FAK), and enhanced migratory activity. Activation of SAPK2/p38 triggered actin polymerization whereas FAX, which was phosphorylated independently of SAPK2/p38, initiated assembly of focal adhesions. Both processes contributed to the formation of stress fibers. Geldanamycin, an inhibitor of HSP90 blocked tyrosine phosphorylation of FAK, assembly of focal adhesions, actin reorganization, and cell, migration, all of which were reversed by overexpressing HSP90. We conclude that VEGFR2 mediates the physiological effect of VEGF on cell migration and that two independent pathways downstream of VEGFR2 regulate actin-based motility. One pathway involves SAPK2/p38 and leads to enhanced actin polymerization activity. The other involves HSP90 as a permissive signal transduction factor implicated in FAK phosphorylation and assembly of focal adhesions.

关键词：肌动蛋白类/生理学抗体/药理学苯醌类钙-钙调素依赖性蛋白激酶类/代谢细胞黏附细胞运动/药物作用细胞运动/生理学细胞培养的细胞支架蛋白质类/生理学内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶激活黏着斑激酶1 黏着斑蛋白酪氨酸激酶类 HSP90热休克蛋白质类/拮抗剂和抑制剂 HSP90热休克蛋白质类/遗传学 HSP90热休克蛋白质类/生理学内酰胺类大环淋巴因子/药理学丝裂原激活蛋白激酶类桩蛋白磷蛋白类/生理学磷酰化蛋白酪氨酸激酶类/拮抗剂和抑制剂蛋白酪氨酸激酶类/代谢原癌基因蛋白质类/生理学醌类/药理学受体蛋白质酪氨酸激酶类/免疫学受体蛋白质酪氨酸激酶类/生理学受体生长因子/免疫学受体生长因子/生理学受体血管内皮生长因子脐静脉血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类纽蛋白/生理学 p38丝裂原活化蛋白激酶类人类

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Actin-based motility of vaccinia virus mimics receptor tyrosine kinase signalling

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NATURE 1999年第6756期401卷 926-929页

作者： Frischknecht, F Moreau, V Röttger, S Gonfloni, S Reckmann, I Superti-Furga, G Way, M European Mol Biol Lab Cell Programme D-69117 Heidelberg Germany European Mol Biol Lab Dev Biol Programme D-69117 Heidelberg Germany

Studies of the actin-based motility of the intracellular pathogens Listeria monocytogenes and Shigella flexneri have provided important insight into the events occurring at the leading edges of motile cells(1-5). Like the bacteria Listeria and Shigella, vaccinia virus, a relative of the causative agent of smallpox, uses actin-based motility to spread between cells(6). In contrast to Listeria or Shigella, the actin-based motility of vaccinia is dependent on an unknown phosphotyrosine protein, but the underlying mechanism remains obscure(7). Here we show that phosphorylation of tyrosine 112 in the viral protein A36R by Src-family kinases is essential for the actin-based motility of vaccinia. Tyrosine phosphorylation of A36R results in a direct interaction with the adaptor protein Nck(8) and the recruitment of the Ena/VASP family member N-WASP(9) to the site of actin assembly. We also show that Nck and N-WASP are essential for the actin-based motility of vaccinia virus. We suggest that vaccinia virus spreads by mimicking the signalling pathways that are normally involved in actin polymerization at the plasma membrane.

关键词：肌动蛋白类/生理学 HeLa细胞外源凝集素类/生理学外源凝集素类 C型膜蛋白质类/遗传学膜蛋白质类/生理学分子模拟磷酰化点突变受体蛋白质酪氨酸激酶类/生理学受体细胞表面/生理学信号传导酪氨酸/代谢痘苗病毒/遗传学痘苗病毒/生理学病毒包膜蛋白质类/遗传学病毒包膜蛋白质类/生理学病毒结构蛋白质类/遗传学病毒结构蛋白质类/生理学 src族激酶类/生理学动物人类小鼠

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Receptor chimeras indicate that the vascular endothelial growth factor receptor-1 (VEGFR-1) modulates mitogenic activity of VEGFR-2 in endothelial cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第22期275卷 16986-16992页

作者： Rahimi, N Dayanir, V Lashkari, K Boston Univ Sch Med Dept Ophthalmol Boston MA 02118 USA Boston Univ Sch Med Dept Biochem Boston MA 02118 USA Harvard Univ Sch Med Schepens Eye Res Inst Boston MA 02114 USA

Vascular endothelial growth factor (VEGF) provokes angiogenesis in vivo and stimulates growth and differentiation of endothelial cells in vitro. Although VEGF receptor-1 (VEGFR-1) and VEGFR-2 are known to be high affinity receptors for VEGF, it is not clear which of the VEGFRs are responsible for the transmission of the diverse biological responses of VEGF. For this purpose we have constructed a chimeric receptor for VEGFR-1 (CTR) and VEGFR-2 (CKR) in which the extracellular domain of each receptor was replaced with the extracellular domain of human colony-stimulating factor-1 receptor (CSF-1R), and these receptors were expressed in pig aortic endothelial (PAE) cells. We show that CHR individually expressed in PAE cells is readily tyrosine-phosphorylated in vivo, autophosphorylated in vitro, and stimulates cell proliferation in a CSF-1-dependent manner. In contrast, CTR individually expressed in PAE cells showed no significant in vivo, in vitro tyrosine phosphorylation and cell growth in response to CSF-1 stimulation. The kinase activity of CKR was essential for its biological activity, since mutation of lysine 866 to arginine abolished its in vivo, in vitro tyrosine phosphorylation and mitogenic signals. Remarkably, activation of CTR repressed CKR-mediated mitogen-activate protein kinase activation and cell proliferation. Similar effects were observed for VEGFR-2 co-expressed with VEGFR-1. Collectively, these findings demonstrate that VEGFR-8 activation plays a positive role in angiogenesis by promoting endothelial cell proliferation In contrast, activation of VEGFR-1 plays a stationary role in angiogenesis by antagonizing VEGFR-2 responses.

关键词：碱基序列 DNA引物内皮血管/细胞学内皮血管/代谢巨噬细胞集落刺激因子/生理学有丝分裂原/代谢有丝分裂原/生理学磷酰化原癌基因蛋白质类/代谢原癌基因蛋白质类/生理学受体蛋白质酪氨酸激酶类/代谢受体蛋白质酪氨酸激酶类/生理学受体生长因子/代谢受体生长因子/生理学受体血管内皮生长因子重组融合蛋白质类/生理学血管内皮生长因子受体1 人类

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Vascular endothelial growth factor-C stimulates the migration and proliferation of Kaposi's sarcoma cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第39期274卷 27617-27622页

作者： Marchiò, S Primo, L Pagano, M Palestro, G Albini, A Veikkola, T Cascone, I Alitalo, K Bussolino, F Univ Turin Sch Med Dept Genet Biol & Biochem Inst Canc Res & Treatment I-10060 Candiolo Italy Univ Turin Sch Med Dept Biomed Sci & Oncol I-10100 Turin Italy Natl Inst Canc Res I-16100 Genoa Italy Ctr Adv Biotechnol I-16100 Genoa Italy Univ Helsinki Haartman Inst Mol Canc Biol Lab SF-00014 Helsinki Finland

Recent evidence suggesting vascular endothelial growth factor-C (VEGF-C), which is a regulator of lymphatic and vascular endothelial development, raised the question whether this molecule could be involved in Kaposi's sarcoma (KS), a strongly angiogenic and inflammatory tumor often associated with infection by human immunodeficiency virus-1. This disease is characterized by the presence of a core constituted of three main populations of "spindle" cells, having the features of lymphatic/vascular endothelial cells, macrophagic/ dendritic cells, and of a mixed macrophage endothelial phenotype. In this study we evaluated the biological response of KS cells to VEGF-C, using an immortal cell line derived from a KS lesion (KS IMM), which retains most features of the parental tumor and can induce KS-like sarcomas when injected subcutaneously in nude mice. We show that VEGFR-3, the specific receptor for VEGF-C, is expressed by KS IMM cells grown in vitro and in vivo. In vitro, VEGF-C induces the tyrosine phosphorylation of VEGFR-2, a receptor also for VEGF-A, as well as that of VEGFR-3. The activation of these two receptors in KS IMM cells is followed by a dose-responsive mitogenic and motogenic response. The stimulation of KS IMM cells with a mutant VEGF-C unable to bind and activate VEFGR-2 resulted in no proliferative response and in a weak motogenic stimulation, suggesting that VEGFR-2 is essential in transducing a proliferative signal and cooperates with VEGFR-3 in inducing cell migration. Our data add new insights on the pathogenesis of KS, suggesting that the involvement of endothelial growth factors may not only determine KS-associated angiogenesis, but also play a critical role in controlling KS cell growth and/or migration and invasion.

关键词：细胞分裂/药物作用细胞培养的趋化作用/药物作用内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学小鼠裸诱变定点磷酰化受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/生理学受体细胞表面/遗传学受体细胞表面/生理学重组蛋白质类/药理学肉瘤卡波西/病理学肉瘤卡波西/病理生理学移植异种肿瘤细胞培养的酪氨酸脐静脉血管内皮生长因子C 血管内皮生长因子受体3 动物人类小鼠

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Selectively desulfated heparin inhibits fibroblast growth factor-induced mitogenicity and angiogenesis

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第32期275卷 24653-24660页

作者： Lundin, L Larsson, H Kreuger, J Kanda, S Lindahl, U Salmivirta, M Claesson-Welsh, L Rudbeck Lab Dept Genet & Pathol S-75185 Uppsala Sweden Biomed Ctr Dept Med Biochem & Microbiol S-75123 Uppsala Sweden Nagasaki Univ Sch Med Nagasaki 8528501 Japan

Fibroblast growth factors (FGFs) are known to induce formation of new blood vessels, angiogenesis. We show that FGF-induced angiogenesis can be modulated using selectively desulfated heparin, Chinese hamster ovary cells (CHO677) deficient in heparan sulfate biosynthesis were employed to assess the function of heparin/heparan sulfate in FGF receptor-1 (FGFR-1) signal transduction and biological responses. In the presence of FGF-2, FGFR-1 kinase and subsequent mitogen-activated protein kinase Erk2 activities were augmented in a dose-dependent manner, whereas high concentrations of heparin resulted in decreased activity. The length of the heparin oligomer, minimally an 8/10-mer, was critical for the ability to enhance FGFR-1 kinase activity, The N- and 2-O-sulfate groups of heparin were essential for binding to FGF-2, whereas stimulation of FGFR-1 and Erk2 kinases by FGF-2 also required the presence of 6-O-sulfate groups. Sulfation at 2-O- and 6-O-positions was moreover a prerequisite for binding of heparin to a lysine-rich peptide corresponding to amino acids 160-177 in the extracellular domain of FGFR-1, Selectively 6-O-desulfated heparin, which binds to FGF-2 but fails to bind the receptor, decreased FGF-2-induced proliferation of CHO677 cells, presumably by displacing intact heparin, Furthermore, FGF-2-induced angiogenesis in chick embryos was inhibited by 6-O-desulfated heparin, Thus, formation of a ternary complex of FGF-2, heparin, and FGFR-1 appears critical for the activation of FGFR-1 kinase and downstream signal transduction. Preventing complex formation by modified heparin preparations may allow regulation of FGF-2 functions, such as induction of angiogenesis.

关键词：尿囊/血液供给氨基酸序列 CHO细胞细胞分裂/药物作用绒毛膜/血液供给仓鼠亚科成纤维细胞生长因子2/拮抗剂和抑制剂成纤维细胞生长因子2/药理学成纤维细胞生长因子2/生理学肝素/化学肝素/药理学类肝素硫酸盐/生物合成类肝素硫酸盐/药理学丝裂原活化蛋白激酶1/代谢分子序列数据新生血管化生理性/药物作用新生血管化生理性/生理学肽碎片/化学合成肽碎片/化学受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/生理学受体成纤维细胞生长因子 1型受体成纤维细胞生长因子/遗传学受体成纤维细胞生长因子/生理学重组蛋白质类/代谢信号传导/药物作用信号传导/生理学构效关系转染动物鸡胚人类

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Ras/MEK/ERK up-regulation of the fibroblast K_Ca channel FIK is a common mechanism for basic fibroblast growth factor and transforming growth factor-β suppression of myogenesis

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13677-13682页

作者： Peña, TL Chen, SH Konieczny, SF Rane, SG Purdue Univ Dept Biol Sci W Lafayette IN 47907 USA

The 10T1/2-MRF4 fibroblast/myogenic cell system was used to address the following interrelated questions: whether distinct signaling pathways underlie myogenic inhibition by basic fibroblast growth factor (bFGF) and transforming growth factor (TGF)-beta;which of these pathways also up-regulates the fibroblast intermediate conductance calcium-activated potassium channel, FIK, a positive regulator of cell proliferation;and whether FIK up-regulation underlies some or all myogenic inhibitory signaling events. The results show that myogenic inhibition in 10T1/2-MRF4 cells, by both bFGF and TGF-beta, requires activation of the Ras/mitogen-activated protein (MAP) kinase/MAP kinase-ERK kinase (MEK)/ extracellular signal-regulated kinase (ERK) pathway, and resultant FIK up-regulation. We show that FIK is instrumental in MEK-dependent suppression of acetylcholine receptor channel expression but that MEK activation and FIK up-regulation are not essential to suppression of myosin heavy chain and myotube formation. These data indicate that Ras/MEK/ERK induction of FIK is pivotal to regulation of certain myogenic events by both receptor tyrosine kinases and TGF-beta receptor, and this is also the first demonstration of chronic FIK upregulation by the TGF-beta receptor family. Furthermore, the results define the physiologic signaling requirements for growth factor-stimulated FIK up-regulation, whereas previous work has concentrated on constitutive FIK up-regulation in cells stably transfected with oncoprotein signaling molecules. This study, together with earlier work showing that FIK positively regulates cell proliferation, establishes this member of the IK channel family as a multifunctional, growth factor-regulated signaling molecule.

关键词：细胞分化/生理学细胞培养的成纤维细胞生长因子2/药理学成纤维细胞/生理学瞬时电导钙激活钾通道肌骨骼/细胞学肌骨骼/生理学钾通道/生理学钾通道钙激活蛋白质丝氨酸苏氨酸激酶/生理学受体蛋白质酪氨酸激酶类/生理学受体 EphA8 小电导钙激活钾通道转化生长因子β/药理学增量调节/药物作用 ras蛋白质类/生理学动物

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Analysis of biological effects and signaling properties of Flt-1 (VEGFR-1) and KDR (VEGFR-2) - A reassessment using novel receptor-specific vascular endothelial growth factor mutants

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第5期276卷 3222-3230页

作者： Gille, H Kowalski, J Li, B LeCouter, J Moffat, B Zioncheck, TF Pelletier, N Ferrara, N Genentech Inc Dept Mol Oncol San Francisco CA 94080 USA Genentech Inc Dept Prot Engn San Francisco CA 94080 USA Genentech Inc Dept Metab & Pharmacokinet San Francisco CA 94080 USA Genentech Inc Dept Prot Chem San Francisco CA 94080 USA

Endothelial cells express two related vascular endothelial growth factor (VEGF) receptor tyrosine kinases, KDR (kinase-insert domain containing receptor, or VEGFR-2) and Flt-1 (fms-like tyrosine kinase, or VEGFR-1). Although considerable experimental evidence links KDR activation to endothelial cell mitogenesis, there is still significant uncertainty concerning the role of individual VEGF receptors for other biological effects such as vascular permeability, VEGF mutants that bind to either KDR or Fit-1 with high selectivity were used to determine which of the two receptors serves to mediate different VEGF functions. In addition to mediating mitogenic signaling, selective KDR activation was sufficient for the activation of intracellular signaling pathways implicated in cell migration. KDR stimulation caused tyrosine phosphorylation of both phosphatidylinositol 3-kinase and phospholipase C gamma in primary endothelial cells and stimulated cell migration. KDR-selective VEGF was also able to induce angiogenesis in the rat cornea to an extent indistinguishable from wild type VEGF, We also demonstrate that KDR, but not Flt-1, stimulation is responsible for the induction of vascular permeability by VEGF.

关键词： 1-磷脂酰肌醇3-激酶/代谢毛细血管通透性/生理学细胞运动/生理学细胞培养的内皮生长因子/代谢内皮血管/细胞学内皮血管/生理学酶激活同工酶类/代谢淋巴因子/代谢丝裂原激活蛋白激酶类/代谢突变新生血管化生理性/生理学磷脂酶Cγ 原癌基因蛋白质类/生理学受体蛋白质酪氨酸激酶类/生理学受体生长因子/生理学受体血管内皮生长因子信号传导/生理学血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类人类

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Enhanced phosphatidylinositol 3-kinase activity and high phosphorylation state of its downstream signalling molecules mediated by Ret with the MEN 2B mutation

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期262卷 68-75页

作者： Murakami, H Iwashita, T Asai, N Shimono, Y Iwata, Y Kawai, K Takahashi, M Nagoya Univ Sch Med Dept Pathol Showa Ku Nagoya Aichi 4668550 Japan

We compared the intracellular signalling pathways through Pet tyrosine kinase activated by glial cell line-derived neurotrophic factor (GDNF), multiple endocrine neoplasia (MEN) 2A, or MEN 2B mutation. Tyrosine phosphorylation of Grb2-associated binder-1 (Gab1) and activation of phosphatidylinositol 3-kinase (PI3-kinase) were induced at higher levels by GDNF stimulation or the MEN 2B mutation than by the MEN 2A mutation. Tyrosine-phosphorylated Gab1 was a major component that interacted with the active PI 3-kinase in vivo. In addition, we found that p62Dok and PKB/Akt were phosphorylated in a PI 3-kinase-dependent manner and the levels of their phosphorylation were significantly higher in the MN 2B transfectant than in the MEN 2A transfectant. Tyrosine phosphorylation of p62Dok resulted in its complex formation with the Pas GTPase-activating protein (Ras-GAP) and the Nck adaptor protein. These findings thus suggested that high levels of activation of PI 3-kinase and of phosphorylation of its downstream signalling molecules may be associated with the clinical phenotype of MEN 2B. (C) 1999 Academic Press.

关键词：衔接蛋白质类信号转导 DNA结合蛋白质类果蝇蛋白质类酶激活/药物作用 GTP酶激活蛋白质类胶质细胞源性神经营养因子胶质细胞源性神经营养因子受体多发性内分泌瘤病2a型/遗传学多发性内分泌瘤病2b型/遗传学突变神经生长因子类神经组织蛋白质类/药理学神经母细胞瘤癌基因蛋白质类/代谢磷酸肌醇3-激酶类/代谢磷蛋白类/代谢磷酰化/药物作用磷酸酪氨酸/代谢蛋白质丝氨酸苏氨酸激酶/代谢蛋白质类/代谢原癌基因蛋白质类/遗传学原癌基因蛋白质类/代谢原癌基因蛋白质类/生理学原癌基因蛋白质c-akt 原癌基因蛋白质c-ret RNA结合蛋白质类受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/代谢受体蛋白质酪氨酸激酶类/生理学信号传导/药物作用转染肿瘤细胞培养的 rasGTP酶激活蛋白质类人类

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G-protein-independent signaling by G-protein-coupled receptors

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TRENDS IN NEUROSCIENCES 2000年第10期23卷 469-475页

作者： Heuss, C Gerber, U Univ Zurich Brain Res Inst CH-8057 Zurich Switzerland

Two classes of receptors transduce neurotransmitter signals: ionotropic receptors and heptahelical metabotropic receptors. Whereas the ionotropic receptors are structurally associated with a membrane channel, a mediating mechanism is necessary to functionally link metabotropic receptors with their respective effecters. According to the accepted paradigm, the first step in the metabotropic transduction process requires the activation of heterotrimeric G-proteins, An increasing number of observations, however, point to a novel mechanism through which neurotransmitters can initiate biochemical signals and modulate neuronal excitability, According to this mechanism metabotropic receptors induce responses by activating transduction systems that do not involve G-proteins.

关键词：基因表达调控异源三聚体GTP结合蛋白质类/生理学无脊椎动物/生理学 MAP激酶信号系统/药物作用模型神经学神经组织蛋白质类/生理学神经递质药/药理学受体蛋白质酪氨酸激酶类/生理学受体生长因子/生理学受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/生理学受体神经递质/分类受体神经递质/药物作用受体神经递质/生理学信号传导/药物作用信号传导/生理学突触传递/药物作用突触传递/生理学转录激活脊椎动物/生理学 src族激酶类/生理学动物人类

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GFRα3, a component of the artemin receptor, is required for migration and survival of the superior cervical ganglion

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NEURON 1999年第4期23卷 725-736页

作者： Nishino, J Mochida, K Ohfuji, Y Shimazaki, T Meno, C Ohishi, S Matsuda, Y Fujii, H Saijoh, Y Hamada, H Osaka Univ Inst Mol & Cellular Biol Div Mol Biol Osaka Japan Japan Sci & Technol Corp Suita Osaka 5650871 Japan Tokyo Metropolitan Inst Med Sci Bunkyo Ku Tokyo 113 Japan Nagoya Univ Sch Agr Sci Lab Anim Genet Chikusa Ku Nagoya Aichi 4648601 Japan

GFR alpha 3 is a component of the receptor for the neurotrophic factor artemin. The role of GFR alpha 3 in nervous system development was examined by generating mice in which the Gfr alpha 3 gene was disrupted. The Gfr alpha 3(-/-) mice exhibited severe defects in the superior cervical ganglion (SCG), whereas other ganglia appeared normal. SCG precursor cells in the mutant embryos failed to migrate to the correct position, and they subsequently failed to innervate the target organs. In wildtype embryos, Gfr alpha 3 was expressed in migrating SCG precursors, and artemin was expressed in and near the SCG. After birth, SCG neurons in the mutant mice underwent progressive cell death. These observations suggest that GFR alpha 3-mediated signaling is required both for the rostral migration of SCG precursors and for the survival of mature SCG neurons.

关键词：细胞死亡/生理学细胞运动/遗传学细胞运动/生理学细胞存活/生理学果蝇蛋白质类基因型免疫组织化学原位杂交小鼠基因敲除神经生长因子类/代谢神经组织蛋白质类/代谢神经元/生理学原癌基因蛋白质类/遗传学原癌基因蛋白质类/生理学原癌基因蛋白质c-ret 受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/生理学受体神经生长因子类/遗传学受体神经生长因子类/代谢颈上神经节/细胞学颈上神经节/胚胎学动物小鼠

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