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Fox, Donald T

Positions:

Assistant Professor of Pharmacology & Cancer Biology

Pharmacology & Cancer Biology
School of Medicine

Assistant Professor in Cell Biology

Cell Biology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 2000

B.S. — College of William and Mary

Ph.D. 2006

Ph.D. — University of North Carolina at Chapel Hill

Grants:

Novel tissue injury regulation at an organ-organ junction

Administered By
Pharmacology & Cancer Biology
AwardedBy
National Institutes of Health
Role
Principal Investigator
Start Date
April 01, 2016
End Date
March 31, 2021

Genetics Training Grant

Administered By
Basic Science Departments
AwardedBy
National Institutes of Health
Role
Mentor
Start Date
September 01, 1979
End Date
June 30, 2020

Organization and Function of Cellular Structure

Administered By
Basic Science Departments
AwardedBy
National Institutes of Health
Role
Mentor
Start Date
July 01, 1975
End Date
June 30, 2020

Pharmacological Sciences Training Program

Administered By
Pharmacology & Cancer Biology
AwardedBy
National Institutes of Health
Role
Participating Faculty Member
Start Date
July 01, 1975
End Date
June 30, 2020

Hypertrophy vs. Proliferation Following Tissue Injury: A Drosophila Model

Administered By
Pharmacology & Cancer Biology
AwardedBy
American Heart Association
Role
Principal Investigator
Start Date
July 01, 2015
End Date
June 30, 2018

Non-Canonical Responses to DNA damage in Drosophila Polyploid Cells

Administered By
Pharmacology & Cancer Biology
AwardedBy
National Institutes of Health
Role
Co-Sponsor
Start Date
March 01, 2015
End Date
February 28, 2018

Training Program in Developmental and Stem Cell Biology

Administered By
Basic Science Departments
AwardedBy
National Institutes of Health
Role
Mentor
Start Date
May 01, 2001
End Date
October 31, 2017

Impact of polyploidy on establishing an HIV-1 reservoir in the kidney

Administered By
Medicine, Infectious Diseases
AwardedBy
University of Alabama at Birmingham
Role
Principal Investigator
Start Date
August 15, 2014
End Date
May 31, 2017

Cancer Biology Training Grant

Administered By
Pharmacology & Cancer Biology
AwardedBy
National Cancer Institute
Role
Mentor
Start Date
July 01, 1993
End Date
March 31, 2016

Examining infection-mediated metastasis with single-cell resolution

Administered By
Pharmacology & Cancer Biology
AwardedBy
National Institutes of Health
Role
Principal Investigator
Start Date
March 01, 2014
End Date
February 29, 2016
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Awards:

Finalist, Emerging Leader Prize. American Society of Cell Biology.

Type
National
Awarded By
American Society of Cell Biology
Date
December 01, 2016

Research Scholar Award. American Cancer Society.

Type
National
Awarded By
American Cancer Society
Date
January 01, 2016

Basil O'Connor Scholar. March of Dimes.

Type
National
Awarded By
March of Dimes
Date
January 01, 2013

Pew Scholars in the Biomedical Sciences. Pew Charitable Trusts, The.

Type
National
Awarded By
Pew Charitable Trusts, The
Date
January 01, 2012

Publications:

Proliferation of Double-Strand Break-Resistant Polyploid Cells Requires Drosophila FANCD2.

Conserved DNA-damage responses (DDRs) sense genome damage and prevent mitosis of broken chromosomes. How cells lacking DDRs cope with broken chromosomes during mitosis is poorly understood. DDRs are frequently inactivated in cells with extra genomes (polyploidy), suggesting that study of polyploidy can reveal how cells with impaired DDRs/genome damage continue dividing. Here, we show that continued division and normal organ development occurs in polyploid, DDR-impaired Drosophila papillar cells. As papillar cells become polyploid, they naturally accumulate broken acentric chromosomes but do not apoptose/arrest the cell cycle. To survive mitosis with acentric chromosomes, papillar cells require Fanconi anemia proteins FANCD2 and FANCI, as well as Blm helicase, but not canonical DDR signaling. FANCD2 acts independently of previous S phases to promote alignment and segregation of acentric DNA produced by double-strand breaks, thus avoiding micronuclei and organ malformation. Because polyploidy and impaired DDRs can promote cancer, our findings provide insight into disease-relevant DNA-damage tolerance mechanisms.

Authors
Bretscher, HS; Fox, DT
MLA Citation
Bretscher, HS, and Fox, DT. "Proliferation of Double-Strand Break-Resistant Polyploid Cells Requires Drosophila FANCD2." Developmental cell 37.5 (June 2016): 444-457.
PMID
27270041
Source
epmc
Published In
Developmental Cell
Volume
37
Issue
5
Publish Date
2016
Start Page
444
End Page
457
DOI
10.1016/j.devcel.2016.05.004

Distinct responses to reduplicated chromosomes require distinct Mad2 responses

Authors
Stormo, BM; Fox, DT
MLA Citation
Stormo, BM, and Fox, DT. "Distinct responses to reduplicated chromosomes require distinct Mad2 responses." ELIFE 5 (May 9, 2016).
Source
wos-lite
Published In
eLife
Volume
5
Publish Date
2016
DOI
10.7754/eLife.15204

The expanding implications of polyploidy.

Polyploid cells, which contain more than two genome copies, occur throughout nature. Beyond well-established roles in increasing cell size/metabolic output, polyploidy can also promote nonuniform genome, transcriptome, and metabolome alterations. Polyploidy also frequently confers resistance to environmental stresses not tolerated by diploid cells. Recent progress has begun to unravel how this fascinating phenomenon contributes to normal physiology and disease.

Authors
Schoenfelder, KP; Fox, DT
MLA Citation
Schoenfelder, KP, and Fox, DT. "The expanding implications of polyploidy." The Journal of cell biology 209.4 (May 2015): 485-491. (Review)
PMID
26008741
Source
epmc
Published In
The Journal of Cell Biology
Volume
209
Issue
4
Publish Date
2015
Start Page
485
End Page
491
DOI
10.1083/jcb.201502016

Indispensable pre-mitotic endocycles promote aneuploidy in the Drosophila rectum.

The endocycle is a modified cell cycle that lacks M phase. Endocycles are well known for enabling continued growth of post-mitotic tissues. By contrast, we discovered pre-mitotic endocycles in precursors of Drosophila rectal papillae (papillar cells). Unlike all known proliferative Drosophila adult precursors, papillar cells endocycle before dividing. Furthermore, unlike diploid mitotic divisions, these polyploid papillar divisions are frequently error prone, suggesting papillar structures may accumulate long-term aneuploidy. Here, we demonstrate an indispensable requirement for pre-mitotic endocycles during papillar development and also demonstrate that such cycles seed papillar aneuploidy. We find blocking pre-mitotic endocycles disrupts papillar morphogenesis and causes organismal lethality under high-salt dietary stress. We further show that pre-mitotic endocycles differ from post-mitotic endocycles, as we find only the M-phase-capable polyploid cells of the papillae and female germline can retain centrioles. In papillae, this centriole retention contributes to aneuploidy, as centrioles amplify during papillar endocycles, causing multipolar anaphase. Such aneuploidy is well tolerated in papillae, as it does not significantly impair cell viability, organ formation or organ function. Together, our results demonstrate that pre-mitotic endocycles can enable specific organ construction and are a mechanism that promotes highly tolerated aneuploidy.

Authors
Schoenfelder, KP; Montague, RA; Paramore, SV; Lennox, AL; Mahowald, AP; Fox, DT
MLA Citation
Schoenfelder, KP, Montague, RA, Paramore, SV, Lennox, AL, Mahowald, AP, and Fox, DT. "Indispensable pre-mitotic endocycles promote aneuploidy in the Drosophila rectum." Development (Cambridge, England) 141.18 (September 2014): 3551-3560.
PMID
25142462
Source
epmc
Published In
Development (Cambridge)
Volume
141
Issue
18
Publish Date
2014
Start Page
3551
End Page
3560
DOI
10.1242/dev.109850

Polyploidization and cell fusion contribute to wound healing in the adult Drosophila epithelium

Background Reestablishing epithelial integrity and biosynthetic capacity is critically important following tissue damage. The adult Drosophila abdominal epithelium provides an attractive new system to address how postmitotic diploid cells contribute to repair. Results Puncture wounds to the adult Drosophila epidermis close initially by forming a melanized scab. We found that epithelial cells near the wound site fuse to form a giant syncytium, which sends lamellae under the scab to re-epithelialize the damaged site. Other large cells arise more peripherally by initiating endocycles and becoming polyploid, or by cell fusion. Rac GTPase activity is needed for syncytium formation, while the Hippo signaling effector Yorkie modulates both polyploidization and cell fusion. Large cell formation is functionally important because when both polyploidization and fusion are blocked, wounds do not re-epithelialize. Conclusions Our observations indicate that cell mass lost upon wounding can be replaced by polyploidization instead of mitotic proliferation. We propose that large cells generated by polyploidization or cell fusion are essential because they are better able than diploid cells to mechanically stabilize wounds, especially those containing permanent acellular structures, such as scar tissue. © 2013 Elsevier Ltd.

Authors
Losick, VP; Fox, DT; Spradling, AC
MLA Citation
Losick, VP, Fox, DT, and Spradling, AC. "Polyploidization and cell fusion contribute to wound healing in the adult Drosophila epithelium." Current Biology 23.22 (November 18, 2013): 2224-2232.
PMID
24184101
Source
scopus
Published In
Current Biology
Volume
23
Issue
22
Publish Date
2013
Start Page
2224
End Page
2232
DOI
10.1016/j.cub.2013.09.029

Endoreplication and polyploidy: insights into development and disease.

Polyploid cells have genomes that contain multiples of the typical diploid chromosome number and are found in many different organisms. Studies in a variety of animal and plant developmental systems have revealed evolutionarily conserved mechanisms that control the generation of polyploidy and have recently begun to provide clues to its physiological function. These studies demonstrate that cellular polyploidy plays important roles during normal development and also contributes to human disease, particularly cancer.

Authors
Fox, DT; Duronio, RJ
MLA Citation
Fox, DT, and Duronio, RJ. "Endoreplication and polyploidy: insights into development and disease." Development 140.1 (January 1, 2013): 3-12. (Review)
PMID
23222436
Source
pubmed
Published In
Development (Cambridge)
Volume
140
Issue
1
Publish Date
2013
Start Page
3
End Page
12
DOI
10.1242/dev.080531

Drosophila Stem Cell Niches: A Decade of Discovery Suggests a Unified View of Stem Cell Regulation

The past decade of research on Drosophila stem cells and niches has provided key insights. Fly stem cells do not occupy a special " state" based on novel " stem cell genes" but resemble transiently arrested tissue progenitors. Moreover, individual stem cells and downstream progenitors are highly dynamic and dispensable, not tissue bulwarks. Niches, rather than fixed cell lineages, ensure tissue health by holding stem cells and repressing cell differentiation inside, but not outside. We review the five best-understood adult Drosophila stem cells and argue that the fundamental biology of stem cells and niches is conserved between Drosophila and mice. © 2011 Elsevier Inc.

Authors
Losick, VP; Morris, LX; Fox, DT; Spradling, A
MLA Citation
Losick, VP, Morris, LX, Fox, DT, and Spradling, A. "Drosophila Stem Cell Niches: A Decade of Discovery Suggests a Unified View of Stem Cell Regulation." Developmental Cell 21.1 (2011): 159-171.
PMID
21763616
Source
scival
Published In
Developmental Cell
Volume
21
Issue
1
Publish Date
2011
Start Page
159
End Page
171
DOI
10.1016/j.devcel.2011.06.018

Error-prone polyploid mitosis during normal Drosophila development

Endopolyploidy arises during normal development in many species when cells undergo endocycles - variant cell cycles in which DNA replicates but daughter cells do not form. Normally, polyploid cells do not divide mitotically after initiating endocycles; hence, little is known about their mitotic competence. However, polyploid cells are found in many tumors, and the enhanced chromosomal instability of polyploid cells in culture suggests that such cells contribute to tumor aneuploidy. Here, we describe a novel polyploid Drosophila cell type that undergoes normal mitotic cycles as part of a remodeling process that forms the adult rectal papillae. Similar polyploid mitotic divisions, but not depolyploidizing divisions, were observed during adult ileum development in the mosquito Culex pipiens. Extended anaphases, chromosome bridges, and lagging chromosomes were frequent during these polyploid divisions, despite normal expression of cell cycle regulators. Our results show that the switch to endocycles during development is not irreversible, but argue that the polyploid mitotic cycle is inherently error-prone, and that polyploid mitoses may help destabilize the cancer genome.

Authors
Fox, DT; Gall, JG; Spradling, AC
MLA Citation
Fox, DT, Gall, JG, and Spradling, AC. "Error-prone polyploid mitosis during normal Drosophila development." Genes and Development 24.20 (2010): 2294-2302.
PMID
20952538
Source
scival
Published In
Genes & development
Volume
24
Issue
20
Publish Date
2010
Start Page
2294
End Page
2302
DOI
10.1101/gad.1952710

The Drosophila Hindgut Lacks Constitutively Active Adult Stem Cells but Proliferates in Response to Tissue Damage

The adult Drosophila hindgut was recently reported to contain active, tissue-replenishing stem cells, like those of the midgut, but located within an anterior ring so as to comprise a single giant crypt. In contrast to this view, we observed no active stem cells and little cell turnover in adult hindgut tissue based on clonal marking and BrdU incorporation studies. Again contradicting the previous proposal, we showed that the adult hindgut is not generated by anterior stem cells during larval/pupal development. However, severe tissue damage within the hindgut elicits cell proliferation within a ring of putative quiescent stem cells at the anterior of the pylorus. Thus, the hindgut does not provide a model of tissue maintenance by constitutively active stem cells, but has great potential to illuminate mechanisms of stress-induced tissue repair. © 2009 Elsevier Inc. All rights reserved.

Authors
Fox, DT; Spradling, AC
MLA Citation
Fox, DT, and Spradling, AC. "The Drosophila Hindgut Lacks Constitutively Active Adult Stem Cells but Proliferates in Response to Tissue Damage." Cell Stem Cell 5.3 (2009): 290-297.
PMID
19699165
Source
scival
Published In
Cell Stem Cell
Volume
5
Issue
3
Publish Date
2009
Start Page
290
End Page
297
DOI
10.1016/j.stem.2009.06.003

Using Bcr-Abl to examine mechanisms by which Abl kinase regulates morphogenesis in Drosophila

Signaling by the nonreceptor tyrosine kinase Abelson (Abl) plays key roles in normal development, whereas its inappropriate activation helps trigger the development of several forms of leukemia. Abl is best known for its roles in axon guidance, but Abl and its relatives also help regulate embryonic morphogenesis in epithelial tissues. Here, we explore the role of regulation of Abl kinase activity during development. We first compare the subcellular localization of Abl protein and of active Abl, by using a phosphospecific antibody, providing a catalog of places where Abl is activated. Next, we explore the consequences for morphogenesis of overexpressing wild-type Abl or expressing the activated form found in leukemia, Bcr-Abl. We find dose-dependent effects of elevating Abl activity on morphogenetic movements such as head involution and dorsal closure, on cell shape changes, on cell protrusive behavior, and on the organization of the actin cytoskeleton. Most of the effects of Abl activation parallel those caused by reduction in function of its target Enabled. Abl activation leads to changes in Enabled phosphorylation and localization, suggesting a mechanism of action. These data provide new insight into how regulated Abl activity helps direct normal development and into possible biological functions of Bcr-Abl. © 2007 by The American Society for Cell Biology.

Authors
Stevens, TL; Rogers, EM; Koontz, LM; Fox, DT; Homem, CCF; Nowotarski, SH; Artabazon, NB; Peifer, M
MLA Citation
Stevens, TL, Rogers, EM, Koontz, LM, Fox, DT, Homem, CCF, Nowotarski, SH, Artabazon, NB, and Peifer, M. "Using Bcr-Abl to examine mechanisms by which Abl kinase regulates morphogenesis in Drosophila." Molecular Biology of the Cell 19.1 (2008): 378-393.
PMID
17959833
Source
scival
Published In
Molecular Biology of the Cell
Volume
19
Issue
1
Publish Date
2008
Start Page
378
End Page
393
DOI
10.1091/mbc.E07-01-0008

Stem cells and their niches: Integrated units that maintain Drosophila tissues

The genetic analysis of four distinct Drosophila stem cells and their niches has revealed principles of stem cell biology that are likely to apply widely. A stem cell and its niche act together as integral parts of a system that supplies replacement cells when and where they are needed within a tissue. Stem cell/niche units are highly regulated and continue to operate despite the periodic turnover and replacement of all of their component cells. To successfully respond to tissue needs, these units receive and process a wide range of local and systemic information. A stem cell alone would be no more use at this task than an isolated neuron. It is only when integrated into a system of multiple interacting cells (the niche) that stem cells achieve the capacity to serve as the fundamental units of tissue homeostasis and repair. ©2008 Cold Spring Harbor Laboratory Press.

Authors
Spradling, AC; Nystul, T; Lighthouse, D; Morris, L; Fox, D; Cox, R; Tootle, T; Frederick, R; Skora, A
MLA Citation
Spradling, AC, Nystul, T, Lighthouse, D, Morris, L, Fox, D, Cox, R, Tootle, T, Frederick, R, and Skora, A. "Stem cells and their niches: Integrated units that maintain Drosophila tissues." Cold Spring Harbor Symposia on Quantitative Biology 73 (2008): 49-57.
PMID
19022764
Source
scival
Published In
Cold Spring Harbor Laboratory: Symposia on Quantitative Biology
Volume
73
Publish Date
2008
Start Page
49
End Page
57
DOI
10.1101/sqb.2008.73.023

Abelson kinase (Abl) and RhoGEF2 regulate actin organization during cell constriction in Drosophila

Morphogenesis involves the interplay of different cytoskeletal regulators. Investigating how they interact during a given morphogenetic event will help us understand animal development. Studies of ventral furrow formation, a morphogenetic event during Drosophila gastrulation, have identified a signaling pathway involving the G-protein Concertina (Cta) and the Rho activator RhoGEF2. Although these regulators act to promote stable myosin accumulation and apical cell constriction, loss-of-function phenotypes for each of these pathway members is not equivalent, suggesting the existence of additional ventral furrow regulators. Here, we report the identification of Abelson kinase (Abl) as a novel ventral furrow regulator. We find that Abl acts apically to suppress the accumulation of both Enabled (Ena) and actin in mesodermal cells during ventral furrow formation. Further, RhoGEF2 also regulates ordered actin localization during ventral furrow formation, whereas its activator, Cta, does not. Taken together, our data suggest that there are two crucial preconditions for apical constriction in the ventral furrow: myosin stabilization/activation, regulated by Cta and RhoGEF2; and the organization of apical actin, regulated by Abl and RhoGEF2. These observations identify an important morphogenetic role for Abl and suggest a conserved mechanism for this kinase during apical cell constriction.

Authors
Fox, DT; Peifer, M
MLA Citation
Fox, DT, and Peifer, M. "Abelson kinase (Abl) and RhoGEF2 regulate actin organization during cell constriction in Drosophila." Development 134.3 (2007): 567-578.
PMID
17202187
Source
scival
Published In
Development (Cambridge)
Volume
134
Issue
3
Publish Date
2007
Start Page
567
End Page
578
DOI
10.1242/dev.02748

Cell Adhesion: Separation of p120's Powers?

The catenin p120 is involved in many processes, including cell-cell adhesion and cancer. Recent work explores whether p120 independently regulates two key binding partners, RhoGTPase and cadherin. © 2007 Elsevier Ltd. All rights reserved.

Authors
Fox, DT; Peifer, M
MLA Citation
Fox, DT, and Peifer, M. "Cell Adhesion: Separation of p120's Powers?." Current Biology 17.1 (2007): R24-R27.
PMID
17208174
Source
scival
Published In
Current Biology
Volume
17
Issue
1
Publish Date
2007
Start Page
R24
End Page
R27
DOI
10.1016/j.cub.2006.11.040

Rho1 regulates Drosophila adherens junctions independently of p120ctn

During animal development, adherens junctions (AJs) maintain epithelial cell adhesion and coordinate changes in cell shape by linking the actin cytoskeletons of adjacent cells. Identifying AJ regulators and their mechanisms of action are key to understanding the cellular basis of morphogenesis. Previous studies linked both p120catenin and the small GTPase Rho to AJ regulation and revealed that p120 may negatively regulate Rho. Here we examine the roles of these candidate AJ regulators during Drosophila development. We found that although p120 is not essential for development, it contributes to morphogenesis efficiency, clarifying its role as a redundant AJ regulator. Rho has a dynamic localization pattern throughout ovarian and embryonic development. It preferentially accumulates basally or basolaterally in several tissues, but does not preferentially accumulate in AJs. Further, Rho1 localization is not obviously altered by loss of p120 or by reduction of core AJ proteins. Genetic and cell biological tests suggest that p120 is not a major dose-sensitive regulator of Rho1. However, Rho1 itself appears to be a regulator of AJs. Loss of Rho1 results in ectopic accumulation of cytoplasmic DE-cadherin, but ectopic cadherin does not accumulate with its partner Armadillo. These data suggest Rho1 regulates AJs during morphogenesis, but this regulation is p120 independent.

Authors
Fox, DT; Homem, CCF; Myster, SH; Wang, F; Bain, EE; Peifer, M
MLA Citation
Fox, DT, Homem, CCF, Myster, SH, Wang, F, Bain, EE, and Peifer, M. "Rho1 regulates Drosophila adherens junctions independently of p120ctn." Development 132.21 (2005): 4819-4831.
PMID
16207756
Source
scival
Published In
Development (Cambridge)
Volume
132
Issue
21
Publish Date
2005
Start Page
4819
End Page
4831
DOI
10.1242/dev.02056

Drosophila p120 catenin plays a supporting role in cell adhesion but is not an essential adherens junction component

Cadherin-catenin complexes, localized to adherens junctions, are essential for cell-cell adhesion. One means of regulating adhesion is through the juxtamembrane domain of the cadherin cytoplasmic tail. This region is the binding site for p120, leading to the hypothesis that p120 is a key regulator of cell adhesion. p120 has also been suggested to regulate the GTPase Rho and to regulate transcription via its binding partner Kaiso. To test these hypothesized functions, we turned to Drosophila, which has only a single p120 family member. It localizes to adherens junctions and binds the juxtamembrane region of DE-cadherin (DE-cad). We generated null alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function. However, p120 mutations strongly enhance mutations in the genes encoding DE-cadherin or Armadillo, the β-catenin homologue. Finally, we examined the localization of p120 during embryogenesis. p120 localizes to adherens junctions, but its localization there is less universal than that of core adherens junction proteins. Together, these data suggest that p120 is an important positive modulator of adhesion but that it is not an essential core component of adherens junctions.

Authors
Myster, SH; Cavallo, R; Anderson, CT; Fox, DT; Peifer, M
MLA Citation
Myster, SH, Cavallo, R, Anderson, CT, Fox, DT, and Peifer, M. "Drosophila p120 catenin plays a supporting role in cell adhesion but is not an essential adherens junction component." Journal of Cell Biology 160.3 (2003): 433-449.
PMID
12551951
Source
scival
Published In
Journal of Cell Biology
Volume
160
Issue
3
Publish Date
2003
Start Page
433
End Page
449
DOI
10.1083/jcb.200211083

Balancing different types of actin polymerization at distinct sites: Roles for Abelson kinase and Enabled

The proto-oncogenic kinase Abelson (Abl) regulates actin in response to cell signaling. Drosophila Abl is required in the nervous system, and also in epithelial cells, where it regulates adherens junction stability and actin organization. Abl acts at least in part via the actin regulator Enabled (Ena), but the mechanism by which Abl regulates Ena is unknown. We describe a novel role for Abl in early Drosophila development, where it regulates the site and type of actin structures produced. In Abl's absence, excess actin is polymerized in apical microvilli, whereas too little actin is assembled into pseudocleavage and cellularization furrows. These effects involve Ena misregulation. In abl mutants, Ena accumulates ectopically at the apical cortex where excess actin is observed, suggesting that Abl regulates Ena's subcellular localization. We also examined other actin regulators. Loss of Abl leads to changes in the localization of the Arp2/3 complex and the formin Diaphanous, and mutations in diaphanous or capping protein 13 enhance abl phenotypes.

Authors
Grevengoed, EE; Fox, DT; Gates, J; Peifer, M
MLA Citation
Grevengoed, EE, Fox, DT, Gates, J, and Peifer, M. "Balancing different types of actin polymerization at distinct sites: Roles for Abelson kinase and Enabled." Journal of Cell Biology 163.6 (2003): 1267-1279.
PMID
14676307
Source
scival
Published In
Journal of Cell Biology
Volume
163
Issue
6
Publish Date
2003
Start Page
1267
End Page
1279
DOI
10.1083/jcb.200307026
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Research Areas:

  • Aneuploidy
  • Cell Cycle
  • Gene Dosage
  • Genome
  • Genomic Instability
  • Image Processing, Computer-Assisted
  • Microscopy, Confocal
  • Polyploidy
  • Transcriptome