-
1.发明授权公开(公告)号：US11279915B2
公开(公告)日：2022-03-22
申请号：US16245298
申请日：2019-01-11
发明人： Aaron C. Brown
摘要： Provided herein are, inter alia, methods, compositions, and kits for producing adipocyte populations such as beige adipocyte populations. Also included are methods and compositions for increasing the level of adipocyte populations (e.g., beige adipocyte populations) in a subject, as well as methods and compositions for treating subjects who are overweight, obese, or who have diabetes.
-
公开(公告)号：US20210100901A1
公开(公告)日：2021-04-08
申请号：US17110543
申请日：2020-12-03
IPC分类号： A61K39/395 , C07K16/18 , A61K38/39 , C07K14/78 , A61P37/04 , A61P35/00 , A61K45/06 , C07K16/28
摘要： The present invention provides antagonists and methods of use thereof in the treatment of cancer and abnormal immune suppression diseases.
-
3.发明授权Therapeutic and diagnostic methods and compositions based on jagged/notch proteins and nucleic acids 失效基于锯齿状/缺口蛋白质和核酸的治疗和诊断方法和组合物公开(公告)号：US07304138B2
公开(公告)日：2007-12-04
申请号：US10650650
申请日：2003-08-28
IPC分类号： C07K14/435 , C07K14/515
CPC分类号： C07K14/705 , A61K38/00 , A61K48/00 , C12N15/1138
摘要： This invention relates to therapeutic and diagnostic methods and compositions based on Jagged/Notch proteins and nucleic acids, and on their role in the signaling pathway relating to endothelial cell migration and/or differentiation. In addition, this invention provides a substantially purified Jagged protein, as well as a substantially purified nucleic acid or segment thereof encoding Jagged protein, or a functionally equivalent derivative, or allelic or species variant thereof. Further, this invention provides a substantially purified soluble Jagged protein and a substantially purified nucleic acid encoding same as well as a recombinant cell comprising a nucleic acid encoding a soluble Jagged protein. Soluble Jagged provides further therapeutic and diagnostic methods relating to diseases, disorders, and conditions involving Jagged/Notch signaling including, inter alia, angiogenesis, differentiation, and control of gene expression.
摘要翻译： 本发明涉及基于Jagged / Notch蛋白质和核酸的治疗和诊断方法和组合物，以及它们在与内皮细胞迁移和/或分化有关的信号传导途径中的作用。 此外，本发明提供了基本上纯化的锯齿状蛋白质，以及编码锯齿状蛋白质的基本上纯化的核酸或其片段，或其功能上等同的衍生物，等位基因或物种变体。 此外，本发明提供了基本上纯化的可溶性Jagged蛋白质和编码其的基本纯化的核酸，以及包含编码可溶性Jagged蛋白质的核酸的重组细胞。 可溶性Jagged提供了与涉及Jagged / Notch信号传导的疾病，病症和病症相关的进一步的治疗和诊断方法，其中尤其包括基因表达的血管发生，分化和控制。
-
4.发明申请Compositions, methods and kits relating to thrombin, Notch signaling and stamatogenesis and growth of stem cells 失效与凝血酶相关的组合物，方法和试剂盒，Notch信号传导和干细胞的发育和生长公开(公告)号：US20060063253A1
公开(公告)日：2006-03-23
申请号：US11209137
申请日：2005-08-22
申请人： Thomas Maciag , Lori Maciag , Vihren Kolev , Joseph Verdi
发明人： Thomas Maciag , Lori Maciag , Vihren Kolev , Joseph Verdi
IPC分类号： C12N5/06
CPC分类号： C12N5/0623 , C12N2501/42 , C12N2501/998
摘要： The present invention relates to methods based on the interactions of thrombin as a biological regulator. More specifically, the invention relates to the interactions of thrombin with regard to Notch signaling, Jagged1, PAR1, and cellular effects mediated thereby. The invention relates to the discovery that thrombin cleaves Jagged1 to produce non-membrane soluble Jagged1 (sJ1). The soluble Jagged1 protein can affect Notch signaling and, among other things, mediate the release of FGF-1 and/or IL-1α from a cell. The invention further relates to the role(s) of thrombin and signaling via Notch proteins and the effect on thrombosis, angiogenesis, and/or differentiation, among other processes. Moreover, the invention relates to discovery that thrombin, sJ1, and TRAP mediate, inter alia, rapid non-classical release of FGF-1, and proteins associated therewith (e.g., p40 Syn1 and S100A13, among others), and the effect growth and proliferation of a stem cell without loss of differentiation potential. Thus, the present invention relates to methods of clonally expanding a pluripotent stem cell while preserving the differentiation potential of the cell, a process termed “stamatogenesis.”
摘要翻译： 本发明涉及基于凝血酶作为生物调节剂的相互作用的方法。 更具体地，本发明涉及凝血酶与Notch信号传导，Jagged1，PAR1以及由此介导的细胞效应的相互作用。 本发明涉及凝血酶切割Jagged1以产生非膜可溶性Jagged1（sJ1）的发现。 可溶性Jagged1蛋白可影响Notch信号传导，其中包括从细胞介导FGF-1和/或IL-1α的释放。 本发明还涉及凝血酶的作用和通过Notch蛋白的信号通路以及其他过程中对血栓形成，血管发生和/或分化的作用。 此外，本发明涉及发现凝血酶，sJ1和TRAP特别介导FGF-1的快速非经典释放和与其相关的蛋白质（例如，p40 Syn1和S100A13等），以及效应生长和 干细胞的增殖而不损失分化潜能。 因此，本发明涉及克隆扩增多能干细胞同时保持细胞的分化潜能的方法，称为“致死生成”的过程。
-
5.发明申请Copper-dependent non-traditional pro-inflammatory cytokine export and methods, compositions and kits relating thereto 审中-公开铜依赖性非传统促炎细胞因子出口及其相关的方法，组合物和试剂盒公开(公告)号：US20040229796A1
公开(公告)日：2004-11-18
申请号：US10786223
申请日：2004-02-23
发明人： Thomas Maciag , Anna Mandinova , Lazar Mandinov , Igor Prudovsky , Stephen Bellum , Raffaella Soldi , Cinzia Bagala
IPC分类号： A61K038/17 , A61K031/555 , A61K031/195
CPC分类号： G01N33/6863 , A61K31/195 , A61K31/28 , A61K31/355 , A61K33/34 , A61K38/1738 , A61K45/06 , G01N33/6869 , G01N2333/545 , G01N2500/10
摘要： The present invention relates to the discovery that non-traditional export of certain pro-inflammatory cytokines lacking a signal sequence from a cell can be inhibited by copper chelation and/or administration to the cell of a truncated form of S100A13 lacking the basic residue portion. Further, copper chelation inhibits, inter alia, neointima formation, macrophage infiltration and associated inflammation, cell proliferation, secretion of extracellular matrix, intimal thickening, adventitial angiogenesis, restenosis, and the like, associated with vascular vessel injury. Thus, the present invention provides novel methods of preventing and treating, and for identifying novel compounds also useful as therapeutics for, such conditions.
摘要翻译： 本发明涉及以下发现：通过对缺乏碱性残基部分的S100A13截短形式的细胞进行铜螯合和/或给药，可以抑制某些缺乏来自细胞的信号序列的促炎细胞因子的非传统出口。 此外，铜螯合尤其抑制与血管损伤相关的新内膜形成，巨噬细胞浸润和相关炎症，细胞增殖，分泌细胞外基质，内膜增厚，外膜血管生成，再狭窄等。 因此，本发明提供了预防和治疗以及用于鉴定也可用作这些病症的治疗剂的新化合物的新方法。
-
6.发明申请公开(公告)号：US20220162557A1
公开(公告)日：2022-05-26
申请号：US17667934
申请日：2022-02-09
发明人： Aaron C. Brown
摘要： Provided herein are, inter alia, methods, compositions, and kits for producing adipocyte populations such as beige adipocyte populations. Also included are methods and compositions for increasing the level of adipocyte populations (e.g., beige adipocyte populations) in a subject, as well as methods and compositions for treating subjects who are overweight, obese, or who have diabetes.
-
7.发明授权Compositions, methods and kits related to thrombin, Notch signaling and stamatogenesis and growth of stem cells 失效与凝血酶相关的组合物，方法和试剂盒，Notch信号传导和干细胞的发育和生长公开(公告)号：US07501281B2
公开(公告)日：2009-03-10
申请号：US11209137
申请日：2005-08-22
发明人： Thomas Maciag
CPC分类号： C12N5/0623 , C12N2501/42 , C12N2501/998
摘要： The present invention relates to methods based on the interactions of thrombin as a biological regulator. More specifically, the invention relates to the interactions of thrombin with regard to Notch signaling, Jagged1, PAR1, and cellular effects mediated thereby. The invention relates to the discovery that thrombin cleaves Jagged1 to produce non-membrane soluble Jagged1 (sJ1). The soluble Jagged1 protein can affect Notch signaling and, among other things, mediate the release of FGF-1 and/or IL-1α from a cell. The invention further relates to the role(s) of thrombin and signaling via Notch proteins and the effect on thrombosis, angiogenesis, and/or differentiation, among other processes. Moreover, the invention relates to discovery that thrombin, sJ1, and TRAP mediate, inter alia, rapid non-classical release of FGF-1, and proteins associated therewith (e.g., p40 Syn1 and S100A13, among others), and the effect growth and proliferation of a stem cell without loss of differentiation potential. Thus, the present invention relates to methods of clonally expanding a pluripotent stem cell while preserving the differentiation potential of the cell, a process termed “stamatogenesis.”
摘要翻译： 本发明涉及基于凝血酶作为生物调节剂的相互作用的方法。 更具体地，本发明涉及凝血酶与Notch信号传导，Jagged1，PAR1以及由此介导的细胞效应的相互作用。 本发明涉及凝血酶切割Jagged1以产生非膜可溶性Jagged1（sJ1）的发现。 可溶性Jagged1蛋白可影响Notch信号传导，其中包括从细胞介导FGF-1和/或IL-1α的释放。 本发明还涉及凝血酶的作用和通过Notch蛋白的信号通路以及其他过程中对血栓形成，血管发生和/或分化的作用。 此外，本发明涉及发现凝血酶，sJ1和TRAP特别介导FGF-1的快速非经典释放和与其相关的蛋白质（例如，p40 Syn1和S100A13等），以及效应生长和 干细胞的增殖而不损失分化潜能。 因此，本发明涉及克隆扩增多能干细胞同时保持细胞的分化潜能的方法，称为“致死生成”的过程。
-
公开(公告)号：US10881732B2
公开(公告)日：2021-01-05
申请号：US15169863
申请日：2016-06-01
IPC分类号： A61K39/395 , A61K39/00 , C07K16/18 , A61K38/39 , C07K14/78 , A61P37/04 , A61P35/00 , A61K45/06 , C07K16/28
摘要： The present invention provides antagonists and methods of use thereof in the treatment of cancer and abnormal immune suppression diseases.
-
9.发明申请Copper-dependent non-traditional pro-inflammatory cytokine export and methods, compositions and kits relating thereto 审中-公开铜依赖性非传统促炎细胞因子出口及其相关的方法，组合物和试剂盒公开(公告)号：US20090123565A9
公开(公告)日：2009-05-14
申请号：US11439397
申请日：2006-05-22
申请人： Thomas Maciag , Lorraine Maciag , Anna Mandinova , Lazar Mandinov , Igor Prudovsky , Stephen Bellum , Raffaella Soldi , Cinzia Bagala
发明人： Thomas Maciag , Lorraine Maciag , Anna Mandinova , Lazar Mandinov , Igor Prudovsky , Stephen Bellum , Raffaella Soldi , Cinzia Bagala
CPC分类号： G01N33/6863 , A61K31/195 , A61K31/28 , A61K31/355 , A61K33/34 , A61K38/1738 , A61K45/06 , G01N33/6869 , G01N2333/545 , G01N2500/10
摘要： The present invention relates to the discovery that non-traditional export of certain pro-inflammatory cytokines lacking a signal sequence from a cell can be inhibited by copper chelation and/or administration to the cell of a truncated form of S100A13 lacking the basic residue portion. Further, copper chelation inhibits, inter alia, neointima formation, macrophage infiltration and associated inflammation, cell proliferation, secretion of extracellular matrix, intimal thickening, adventitial angiogenesis, restenosis, and the like, associated with vascular vessel injury. Thus, the present invention provides novel methods of preventing and treating, and for identifying novel compounds also useful as therapeutics for, such conditions.
摘要翻译： 本发明涉及以下发现：通过对缺乏碱性残基部分的S100A13截短形式的细胞进行铜螯合和/或给药，可以抑制某些缺乏来自细胞的信号序列的促炎细胞因子的非传统出口。 此外，铜螯合尤其抑制与血管损伤相关的新内膜形成，巨噬细胞浸润和相关炎症，细胞增殖，分泌细胞外基质，内膜增厚，外膜血管生成，再狭窄等。 因此，本发明提供了预防和治疗以及用于鉴定也可用作这些病症的治疗剂的新化合物的新方法。
-
10.发明申请Compositions, methods and kits relating to CTHRC1, a novel modulator of collagen matrix 审中-公开与CTHRC1相关的组合物，方法和试剂盒，胶原蛋白基质的新型调节剂公开(公告)号：US20050147602A1
公开(公告)日：2005-07-07
申请号：US10939233
申请日：2004-09-10
申请人： Volkhard Lindner
发明人： Volkhard Lindner
IPC分类号： C07K14/51 , A01K67/00 , A61K39/00 , A61K39/395 , C07H21/04 , C07K14/785
CPC分类号： C07K14/78 , A01K67/0275 , A01K2217/05 , A01K2227/105 , A01K2267/035 , A61K38/00 , A61K2039/505 , C07K14/4702 , C07K14/51 , C07K16/18 , C07K2319/00 , C07K2319/41 , C07K2319/60 , C12N15/8509
摘要： The invention relates to a novel CTHRC1 nucleic acid and protein encoded thereby. Expression of CTHRC1 is induced by injury in, among others, arteries and skin, and CTHRC1 is expressed in bone, cartilage, kidney, lung and brain. CTHRC1 expression is associated with collagen matrix production, arterial remodeling, arterial restenosis, constrictive remodeling, vessel injury, ectopic ossification, fibrosis, and the like. CTHRC1 also plays a role in cell-cell and cell-matrix adhesion, cell-migration, and bone, cartilage, skin and brain development. CTHRC1 also regulates the level of BMPs, including BMP1 and BMP4, and the invention encompasses methods relating to affecting the level of BMPs by affecting the level of CTHRC1. In addition, the invention relates to modulation of the level of CTHRC1 to affect processes associated with fibrosis mediated by formation of collagen matrix. The invention further relates to methods of treating, preventing, and/or detecting these diseases, disorders or conditions, where the methods comprise modulating or detecting CTHRC1 expression and/or production of CTHRC1 polypeptide. The invention also relates to affecting CTHRC1 expression using cytokines.
摘要翻译： 本发明涉及由此编码的新型CTHRC1核酸和蛋白质。 CTHRC1的表达是由动脉和皮肤等损伤引起的，CTHRC1在骨，软骨，肾，肺和脑中表达。 CTHRC1表达与胶原基质产生，动脉重塑，动脉再狭窄，缩窄重塑，血管损伤，异位骨化，纤维化等有关。 CTHRC1也在细胞和细胞 - 基质粘附，细胞迁移和骨，软骨，皮肤和脑发育中发挥作用。 CTHRC1还规定BMPs（包括BMP1和BMP4）的水平，本发明包括通过影响CTHRC1水平影响BMP水平的方法。 此外，本发明涉及调节CTHRC1的水平以影响与形成胶原基质介导的纤维化相关的过程。 本发明还涉及治疗，预防和/或检测这些疾病，病症或病症的方法，其中所述方法包括调节或检测CTHRC1表达和/或产生CTHRC1多肽。 本发明还涉及使用细胞因子影响CTHRC1表达。
-
-
-
-
-
-
-
-
-
搜索结果
22 条记录 (耗时 0.02 秒)
