James L. Sherley

Dr. James L. Sherley

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Research Focus & Metrics

Academic Career Length

29Years (1998-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 November 2002 in Stem Cells
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JSJames L. Sherley
James L. Sherley
A singular challenge in stem cell research today is the expansion and propagation of functional adult stem cells. Unlike embryonic stem cells, which are immortal in culture, adult stem cells are notorious for the difficulty encountered when attempts are made to expand them in culture. One overlooked reason for this difficulty may be the inherent asymmetric cell kinetics of stem cells in postnatal somatic tissues. Senescence is the expected fate of a culture whose growth depends on adult stem cells that divide with asymmetric cell kinetics. Therefore, the bioengineering of strategies to expand adult stem cells in culture requires knowledge of cellular mechanisms that control asymmetric cell kinetics. The properties of several genes recently implicated to function in a cellular pathway(s) that regulates asymmetric cell kinetics are discussed. Understanding the function of these genes in asymmetric cell kinetics mechanisms may be the key that unlocks the adult stem cell expansion problem.

1 January 2001 in BioMed Research International
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Journal Article
Open access
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LRLakshmi Rambhatla
Lakshmi Rambhatla
SBShirley A. Bohn
Shirley A. Bohn
PSPatrizia B. Stadler
Patrizia B. Stadler
JBJonathan T. Boyd
Jonathan T. Boyd
RCRonald A. Coss
Ronald A. Coss
JSJames L. Sherley
James L. Sherley
Although senescence is a defining property of euploid mammalian cells, its physiologic basis remains obscure. Previously, cell kinetics properties of normal tissue cells have not been considered in models for senescence. We now provide evidence that senescence is in fact the natural consequence of normal in vivo somatic stem cell kinetics extended in culture. This concept of senescence is based on our discovery that cells engineered to conditionally express the well-recognized tumor suppressor protein and senescence factor, p53, exhibit asymmetric cell kinetics. In vivo, asymmetric cell kinetics are essential for maintenance of somatic stem cells; ex vivo, the same cell kinetics yield senescence as a simple kinetic endpoint. This new “asymmetric cell kinetics model” for senescence suggests novel strategies for the isolation and propagation of somatic tissue stem cells in culture.

24 July 2003 in Biotechnology and Bioengineering
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Journal Article
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HLHsuan‐Shu Lee
Hsuan‐Shu Lee
GCGracy G. Crane
Gracy G. Crane
JMJoshua R. Merok
Joshua R. Merok
JTJames R. Tunstead
James R. Tunstead
NHNicole L. Hatch
Nicole L. Hatch
JSJames L. Sherley
James L. Sherley

1 December 2002
Verified
Journal Article
Closed access
JMJoshua R Merok
Joshua R Merok
JLJanice A Lansita
Janice A Lansita
JTJames R Tunstead
James R Tunstead
JSJames L. Sherley
James L. Sherley

1 January 2001 in BioMed Research International
Verified
Journal Article
Open access
PDF file
JMJoshua R. Merok
Joshua R. Merok
JSJames L. Sherley
James L. Sherley
Here we have reviewed the conventional definitions and fundamental characteristics of the two basic types of stem cells, embryonic stem cells (ESCs) and somatic stem cells (SSCs). By taking into account the often‐overlooked asymmetric cell kinetics of SSCs, we consider the evidence that should SSCs retain these growth kinetics in vitro, a natural kinetic barrier to SSC propagation exists. Recent discoveries showing that the tumor suppressor gene p53 can act as a regulator of asymmetric cell kinetics provide a target pathway for in vitro SSC propagation strategies.

1 November 1998 in Journal of Cellular Physiology
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Journal Article
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YLYuan Liu
Yuan Liu
LRLee B. Riley
Lee B. Riley
SBShirley A. Bohn
Shirley A. Bohn
JBJudith A. Boice
Judith A. Boice
PSPatrizia B. Stadler
Patrizia B. Stadler
JSJames L. Sherley
James L. Sherley