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Author Topic:   keloids
ereichen
Member
posted 07-07-2001 12:15 AM     Click Here to See the Profile for ereichen   Click Here to Email ereichen     Edit/Delete Message Reply w/Quote
Dear Colleagues,

We work on the identification of genes that cause familial keloid formation. We are looking for multi-generation families for linkage analysis and welcome collaborations from clinicians or researchers who can provide such families or can help us identify families with several affected members.

Ernst Reichenberger Ph.D.
University of Connecticut
263 Farmington Ave
Farmington CT 06030-3705

Tel 860-679-2062
Fax 860-679-2910
email reichenberger@uchc.edu
www.keloids.org

[This message has been edited by Administrator (edited 02-13-2003).]

IP: 199.93.248.226

Ammar Elshiekh
Member
posted 01-28-2003 09:23 PM     Click Here to See the Profile for Ammar Elshiekh   Click Here to Email Ammar Elshiekh     Edit/Delete Message Reply w/Quote
quote:
Originally posted by ereichen:
Dear Colleagues,

We work on the identification of genes that cause familial keloid formation. We are looking for multi-generation families for linkage analysis and welcome collaborations from clinicians or researchers who can provide such families or can help us identify families with several affected members.

Ernst Reichenberger Ph.D.
Harvard-Forsyth Department of Oral Biology
HSDM, Forsyth Institute
140 The Fenway
Boston, MA 02115

Tel 617-456-7717
Fax 617-437-9822
email ereichenberger@forsyth.org
www.forsyth.org



Dear Dr. ;

Hello , and happy new a year. I'm glad to write for you. I'm sudanese graduate.

I would like to work in the subject of Keloid formation.

From many studies found ; Keloids are benign collagenous tumor caused by abnormal healnig . The TGF-B. &IL-1regulate the iNOS,the importance of this in relation to keloid formation is that NO was recently proven activate collagenase, which are responsible for collagen metabolism .The TGF-B. also activate collagen synthase. And also a recent study comparing iNOS activity & expression in stratum basale of normal skin , scar and keloids established that iNOS activity & _expression in keloids was reduced compared to normal skin.

From these results lead to the cause of keloid formation.

In other feature,the important new insights have been gained into signal transduction pathways down stream of the receptor serine-threonine kinases of ligands belonging to the TGF-B. superfamily. A novel family of protiens called SMADs. ,act as latent transcriptional activators in that they're phosphorylated directly bythe receptor kinase and then hetromeric complex with a common mediator,smad4,translocate to the nucleus where they participate in DNA-bound complexes to activate transcription of target genes.

Smad4 [phosphoprotein] forms a complex with DNA-binding domain containing promrter and there by activates transcription of target gene [protien repressor of iNOS] ,i.e TGF-B. has both, activate collagen expression and inhibit collagenase via iNOS.

From these above , I proposed to study this phenomenon under the title : TGF-B. & IL-1 genes Susceptibility to Development of Keloid in Sudanese Population.

The objective of my research is to gain insight into mechanisms of TGF-B. action by study of SMAD-interacting protein and altered interacting might play in keloid formation.

My objective is currently focused on several diffrent aspects of SMAD-interacting protein ,in thenucleus, from TGF-B. superfamily ligands ,with the long-term goal of integrating insights provided from in vitro studies, often by necessity in overexpression systems, into an understanding of the roles of particular smad4-interacting protein in vivo in normal physiology and ultimately keloid pathogenesis.

I would be glad if you agree to supervise my work , or any other supervisor suggest for me.

with best regards

Ammar Elshiekh


IP: 212.0.153.234

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