The role of KIT ligand CXC chemokine receptor CXCR4, fibroblast growth factors and
their receptors (FGFRs), Notch or its ligand Jagged1 and retinoic acid (RA) signaling
in determining the fate of these cells in the regulation of normal hematopoietic stem
cells is well-known An increasing amount of evidence from experimental and computational
bioinformatic analysis suggests that there are many domains in DNA sequences that
remain evolutionarily conserved. In some cases, these conserved patterns in a collection
of unaligned DNA and protein sequences present the same functional and regulatory
properties and are significant for the molecular role of these sequences. Discriminative
motif finding algorithms aim to increase the sensitivity and selectivity of conserved
motif discovery by utilizing a specific set of DNA and protein sequences, and searching
for binding sites and homolog repeats among the sets of the selected sequences. In
the present study we introduce a combined bioinformatic software-based discriminative
methodology to detect short, highly and most conserved motifs between the DNA sequences
within the FLT3, CXCR4, CKIT, HOXB4, JAGGED1, FGF1 proteins and then, on finding out
a multi-target motif conserved featured superagonist peptide about them including
their physical regulatory properties, as well as their function as an ex-vivo positive
modulator for the enhancement of human stem cell expansion rates.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to CytotherapyAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
Article info
Publication history
199
Identification
Copyright
© 2014 Published by Elsevier Inc.