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Qingning N Su

from Germantown, MD
Age ~68
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Also known as:
Qing Ning Su, Qing N Su, Quingning Su, Su Qingning
Phone and address:
20813 Amber Ridge Dr, Germantown, MD 20876
(301) 916-8296
Related to:
Jin Kyung Kim, 77Hsiang L Kuo, 53Sun Lee, 85Martin Sullivan, 45Roy Kuo
Connected to:
Ah B Su, 43Alan S Su, 39Alan W Su, 51Albert Su, 40Angie Y Su, 69Ann P Su, 67Can Y Su, 77Chian Y Su, 47Chiayi Su, 38Darren K Su, 29

Qingning Su Phones & Addresses

  • 20813 Amber Ridge Dr, Germantown, MD 20876 (301) 916-8296
  • 263 Congressional Pkwy, Rockville, MD 20852 (301) 468-8138
  • Bethesda, MD

Work

Position: Professional/Technical

Education

Degree: High school graduate or higher

Publications

Us Patents

Himf And Btk In Pulmonary, Cardiac And Inflammation Disorders

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US Patent:
20100028355, Feb 4, 2010
Filed:
Dec 18, 2007
Appl. No.:
12/518857
Inventors:
Roger A. Johns - Reisterstown MD, US
Qingning Su - Germantown MD, US
Hunter Clay Champion - Baltimore MD, US
Assignee:
The Johns Hopkins University - Baltimore MD
International Classification:
A61K 39/395
A61K 31/7052
G01N 33/53
G01N 33/68
A61P 11/00
C12Q 1/02
A61P 29/00
US Classification:
4241391, 514 44 A, 436501, 436 86, 435 792, 435 29
Abstract:
Hypoxia induced mitogenic factor (HIMF) is a member of the “found in inflammatory zone” (FIZZ)/resistin family of proteins and has potent mitogenic, angiogenic, and vasoconstrictive effects in the lung vasculature. The receptor/binding partners for this family of proteins have been largely unknown. We identified Bruton's tyrosine kinase (BTK) as a functional HIMF binding partner through GST-HIMF pull-downs and mass spectrometry. Using primary cultured HIMF-stimulated murine bone marrow cells, we demonstrated that BTK was recruited to the leading edge of the cells. We also demonstrated that BTK and the closely related tyrosine kinase Fyn, colocalized at the growth cone process in these cells. HIMF stimulation induced BTK autophosphorylation, which peaked at 2.5 minutes. A transwell migration assay showed that treatment with recombinant murine HIMF induced migration of primary cultured bone marrow cells, which was completely blocked by the BTK inhibitor, LFM-A13. In vivo studies, using the rat hindlimb ischemia model, revealed that HIMF can stimulate angiogenesis in the hypoxic tissue probably through inducing the migration of endothelial progenitor cells (EPCs) to areas of active angiogenesis. Our results indicate that HIMF may acts as a chemotactic molecule in stimulating the migration of leukocytes/EPCs from bone marrow to targeted tissues through activation of the BTK pathway.

Anti-Himf Antibodies To Treat Lung Diseases

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US Patent:
20140080151, Mar 20, 2014
Filed:
Nov 29, 2012
Appl. No.:
13/688439
Inventors:
Qingning Su - Germantown MD, US
Hunter Clay Champion - Baltimore MD, US
Assignee:
THE JOHNS HOPKINS UNIVERSITY - Baltimore MD
International Classification:
G01N 33/543
US Classification:
435 792
Abstract:
Hypoxia induced mitogenic factor (HIMF) is a member of the “found in inflammatory zone” (FIZZ)/resistin family of proteins and has potent mitogenic, angiogenic, and vasoconstrictive effects in the lung vasculature. The receptor/binding partners for this family of proteins have been largely unknown. We identified Bruton's tyrosine kinase (BTK) as a functional HIMF binding partner through GST-HIMF pull-downs and mass spectrometry. Using primary cultured HIMF-stimulated murine bone marrow cells, we demonstrated that BTK was recruited to the leading edge of the cells. A transwell migration assay showed that treatment with recombinant murine HIMF induced migration of primary cultured bone marrow cells, which was completely blocked by a BTK inhibitor. In vivo studies revealed that HIMF can stimulate angiogenesis in the hypoxic tissue. Our results indicate that HIMF may act as a chemotactic molecule in stimulating the migration of leukocytes/EPCs from bone marrow to targeted tissues through activation of the BTK pathway.

Anti-Himf Antibodies To Treat Lung Diseases

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US Patent:
20170276688, Sep 28, 2017
Filed:
Dec 8, 2016
Appl. No.:
15/372906
Inventors:
- Baltimore MD, US
Qingning Su - Germantown MD, US
Hunter Clay Champion - Baltimore MD, US
International Classification:
G01N 33/68
G01N 33/74
G01N 33/543
C07K 16/40
C07K 14/47
C07K 16/18
C12N 9/12
Abstract:
Hypoxia induced mitogenic factor (HIMF) is a member of the “found in inflammatory zone” (FIZZ)/resistin family of proteins and has potent mitogenic, angiogenic, and vasoconstrictive effects in the lung vasculature. The receptor/binding partners for this family of proteins have been largely unknown. We identified Bruton's tyrosine kinase (BTK) as a functional HIMF binding partner through GST-HIMF pull-downs and mass spectrometry. Using primary cultured HIMF-stimulated murine bone marrow cells, we demonstrated that BTK was recruited to the leading edge of the cells. We also demonstrated that BTK and the closely related tyrosine kinase Fyn, colocalized at the growth cone process in these cells. HIMF stimulation induced BTK autophosphorylation, which peaked at 2.5 minutes. A transwell migration assay showed that treatment with recombinant murine HIMF induced migration of primary cultured bone marrow cells, which was completely blocked by the BTK inhibitor, LFM-A13. In vivo studies, using the rat hindlimb ischemia model, revealed that HIMF can stimulate angiogenesis in the hypoxic tissue probably through inducing the migration of endothelial progenitor cells (EPCs) to areas of active angiogenesis. Our results indicate that HIMF may acts as a chemotactic molecule in stimulating the migration of leukocytes/EPCs from bone marrow to targeted tissues through activation of the BTK pathway.

Methods For Diagnosing Pulmonary Hypertension

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US Patent:
20150276761, Oct 1, 2015
Filed:
Apr 3, 2015
Appl. No.:
14/678213
Inventors:
- Baltimore MD, US
Qingning Su - Germantown MD, US
Hunter Clay Champion - Baltimore MD, US
International Classification:
G01N 33/68
C07K 16/18
Abstract:
Hypoxia induced mitogenic factor (HIMF) is a member of the “found in inflammatory zone” (FIZZ)/resistin family of proteins and has potent mitogenic, angiogenic, and vasoconstrictive effects in the lung vasculature. The receptor/binding partners for this family of proteins have been largely unknown. We identified Bruton's tyrosine kinase (BTK) as a functional HIMF binding partner through GST-HIMF pull-downs and mass spectrometry. Using primary cultured HIMF-stimulated murine bone marrow cells, we demonstrated that BTK was recruited to the leading edge of the cells. We also demonstrated that BTK and the closely related tyrosine kinase Fyn, colocalized at the growth cone process in these cells. HIMF stimulation induced BTK autophosphorylation, which peaked at 2.5 minutes. A transwell migration assay showed that treatment with recombinant murine HIMF induced migration of primary cultured bone marrow cells, which was completely blocked by the BTK inhibitor, LFM-A13. In vivo studies, using the rat hindlimb ischemia model, revealed that HIMF can stimulate angiogenesis in the hypoxic tissue probably through inducing the migration of endothelial progenitor cells (EPCs) to areas of active angiogenesis. Our results indicate that HIMF may acts as a chemotactic molecule in stimulating the migration of leukocytes/EPCs from bone marrow to targeted tissues through activation of the BTK pathway.
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Qingning N Su from Germantown, MD, age ~68 Get Report