Protein Production
293FT, 293E, CHO

Truly Functional Protein
95% Purity
1-10 mg in 2 weeks

GeneExpressoMax™
293Expresso™

Transfection Reagents
* 90% Efficiency
* 95% Viability
* No sera interference
* Simple protocol
* High-throughput
* Only $98/ml

Baculovirus
Functional Protein
95% Purity
Fast turnaround
1-10 mg from Sf9 cells

Adenovirus, AAV
& Lentivirus

ORF or shRNA
* High Titer
* Cre, FLP, ΦC31
* Protein Kinases
* Transcription Factors
* Luciferases, GFP, RFP
* Protein Production
* Stable Cell Line


Excellgen

Christina B Whiteus
Northwestern University At Chicago

Project start date: 2010-01-01

Project end date: 2012-12-31


Sponsored Links Excellgen http://Excellgen.com

Transient Protein Expression in CHO and HEK293 Cells
Transient Expression, Truly Functional Protein, 95% purity, 1~20 mg, fast turnaround. $5500, $3950
Baculovirus Protein Expression
Fast turn around, >95% purity functional protein. No outsourcing to China or India. $5500, $3950
Recombinant Lentivirus & Adenovirus
High Yield and High Titer up to 1010 (lentivirus) and 1013 (adenovirus) for Guaranteed Expression of GOI. $3000, $2500

Christina B Whiteus
Northwestern University

Project start date: 2010-01-01

Project end date: 2012-12-31



Grants awarded to Christina B Whiteus

THE MECHANISMS AND ROLE OF POSTNATAL CEREBRAL VASCULAR REMODELING

Christina B Whiteus
Northwestern University, 750 N. Lake Shore Drive, 7th, Chicago, Il 60611

Grant 1F31NS068041-01 from National Institute Of Neurological Disorders And Stroke

Abstract: Cerebral blood flow is tightly regulated to meet the brain´s large energetic needs. Yet it remains unclear how a precise matching between the degree of vascularization and regional metabolic demands is achieved during development. The brain´s energetic needs increase dramatically in the early postnatal period due to massive synaptogenesis. However, the process of postnatal vascular remodeling, which could be critical for establishing an adequate vascular network, remains poorly understood. This proposal aims at increasing our understanding of postnatal vascular remodeling. We hypothesize that neuronal activity promotes postnatal vascular remodeling via vascular endothelial growth factor (VEGF) and that transient disruption of this process has permanent consequences on neuronal connectivity. To test this, we will use a variety of genetic and pharmacological methods to alter neuronal activity as well as vascular and neuronal imaging in fixed tissues and the living mouse brain using two-photon microscopy. In specific aim 1, we characterize the patterns of vascular remodeling by measuring the degree of angiogenesis, sprouting and pruning and correlate it with regional synaptic density. In aim 2, we determine the effects of neuronal activity on vascular remodeling by altering neuronal activity using pharmacological and genetic methods. We also measure the effect of neuronal activity on levels of VEGF. In aim 3, we determine the effects of altering postnatal vascular remodeling on neuronal structure and connectivity. Additionally, we test whether vascular remodeling occurs within a critical period analogous to that observed with postnatal refinement of neuronal connections. Together, these studies will greatly advance our understanding of the mechanisms of postnatal vascular remodeling which may be critically important in meeting the metabolic demands of the brain and maintaining the health of neurons

Keywords: Action Potentials; Age; Angiogenesis Inhibition; Angiogenic Inhibition; Area; Asses; Astrocytes; Astrocytus; Astroglia; Blood Vessels; Botulin; Botulinum Toxins; Brain; Cell Function; Cell Growth in Number; Cell Multiplication; Cell Process; Cell Proliferation; Cell physiology; Cells; Cellular Function; Cellular Physiology; Cellular Process; Cellular Proliferation; Cerebrovascular Circulation; Cerebrum; Chloride Channels; Clostridium botulinum Toxins; Clostridium tetani Toxin; Confocal Microscopy; D-Glucose; Development; Dextrose; Donkey; Effects, Longterm; Embryo Development; Embryogenesis; Embryonic Development; Encephalon; Encephalons; Endothelial Cells; Epilepsy; Epileptic Seizures; Epileptics; Equus asinus; Exercise; Exercise, Physical; Future; GFP; Genetic; Glucose; Goals; Green Fluorescent Proteins; Health; Image; Injection of therapeutic agent; Injections; Ion Channels, Chloride; Life; Long-Term Effects; Mammals, Mice; Measures; Metabolic; Methods; Methods and Techniques; Methods, Other; Mice; Mice, Transgenic; Microscopy; Microscopy, Confocal; Modeling; Monitor; Motor Cortex; Murine; Mus; Nature; Neonatal; Nerve Cells; Nerve Unit; Nervous System, Brain; Neural Cell; Neurocyte; Neurons; O element; O2 element; Organ; Oxygen; Pattern; Pharmacological Treatment; Process; Proteins; Role; Seizure Disorder; Slice; Spinal Column; Spine; Staging; Stereotyping; Structure; Subcellular Process; Synapses; Synaptic; System; System, LOINC Axis 4; Techniques; Testing; Tetanus Toxin; Time; Transgenic Mice; VEGFs; Vascular Endothelial Growth Factors; Vascular remodeling; Vascularization; Vegf; Vertebral column; angiogenesis; backbone; cell type; cerebral blood flow; cerebral circulation; cerebrocirculation; critical period; density; epilepsia; epileptiform; epileptogenic; experiment; experimental research; experimental study; gene product; imaging; in vivo; inhibitor; inhibitor/antagonist; meetings; neonate; neuron cell death; neuron loss; neuronal; neuronal cell death; neuronal loss; postnatal; research study; response; social role; synapse formation; synaptogenesis; tissue fixing; treatment effect; two-photon; vascular

Project start date: 2010-01-01

Project end date: 2012-12-31

Budget start date: 1-JAN-2010

Budget end date: 31-DEC-2010

PFA/PA: PA-07-106

1F31NS068041-01 (2010): $31609