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Article: Ectopic localization of mitochondrial ATP synthase: a target for anti-angiogenesis intervention?

Kenan, Daniel J / Wahl, Miriam L

Journal of bioenergetics and biomembranes

2006 Volume 37, Issue 6, Page(s) 461–465

Abstract: ... with intracellular pH regulation (Wahl and Grant, 2002; Wahl et al., 2002). Although angiostatin administered ...

Abstract	A receptor for angiostatin was identified on the surface of endothelial cells as F(1)-F(0) ATP synthase (Moser et al., 1999). Proc. Natl. Acad. Sci. U.S.A. 96, 2811-2816. This ectopic ATP synthase catalyzes ATP synthesis and is inhibited by angiostatin over a wide pH range. Endothelial cells grown at normal pH suffer no ill effects from this angiostatin-mediated inhibition of ATP synthase, whereas endothelial cells grown at low, tumor-like extracellular pH cannot maintain a normal intracellular pH and die. Angiostatin inhibits both ATP synthesis and ATP hydrolysis (Moser et al., 2001) and interferes with intracellular pH regulation (Wahl and Grant, 2002; Wahl et al., 2002). Although angiostatin administered intravenously is cleared from the circulation in a matter of minutes, angiostatin-mimetics that are more stable have potential for clinical application. An angiostatin-mimetic activity has recently been observed using a polyclonal antibody against the beta catalytic subunit of ATP synthase. In order to explore the mechanism of action of angiostatin and its mimetics, further work needs to be done to evaluate clinical applicability, specificity, and contraindications for this class of therapeutics.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/therapeutic use ; Angiostatins/pharmacology ; Angiostatins/therapeutic use ; Antineoplastic Agents ; Endothelial Cells/drug effects ; Humans ; Mitochondrial Proton-Translocating ATPases/antagonists & inhibitors
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents ; Angiostatins (86090-08-6) ; Mitochondrial Proton-Translocating ATPases (EC 3.6.3.-)
Language	English
Publishing date	2006-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	198499-8
ISSN	1573-6881 ; 0145-479X ; 0449-5705
ISSN (online)	1573-6881
ISSN	0145-479X ; 0449-5705
DOI	10.1007/s10863-005-9492-x
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Article: Angiostatin and anti-angiogenic therapy in human disease.

Wahl, Miriam L / Moser, Tammy L / Pizzo, Salvatore V

Recent progress in hormone research

2004 Volume 59, Page(s) 73–104

Abstract: Many diseases have abnormal quality and/or quantity of vascularization as a characteristic feature. Cancer cells elicit the growth of new capillaries during neovascularization in a process termed angiogenesis. In diabetics, pathologic angiogenesis in ... ...

Abstract	Many diseases have abnormal quality and/or quantity of vascularization as a characteristic feature. Cancer cells elicit the growth of new capillaries during neovascularization in a process termed angiogenesis. In diabetics, pathologic angiogenesis in various tissues is a clinical feature of many common complications. Therefore, the diabetic cancer patient warrants special consideration and extra care in the design of anti-angiogenic treatments without adverse side effects. Some treatment regimens that look promising in vitro, in animal models, or in early clinical trials may be contra-indicated for diabetics. This chapter will review the common complications of diabetes, with emphasis on the angiogenic pathology. Recent research related to the mechanism of action and basis for specificity of the anti-angiogenic peptide, angiostatin, will be the focus. The aim is to shed light on areas in which more research is needed with respect to angiostatin and other anti-angiogenic agents and the microenvironmental conditions that affect their activities, in order to develop improved therapeutic strategies for diabetic cancer patients.
MeSH term(s)	Angiostatins/chemistry ; Angiostatins/metabolism ; Angiostatins/therapeutic use ; Animals ; Diabetes Complications ; Diabetic Retinopathy ; Disease Models, Animal ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiopathology ; Humans ; Neoplasms/blood supply ; Neoplasms/complications ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/physiopathology
Chemical Substances	Angiostatins (86090-08-6)
Language	English
Publishing date	2004-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	209338-8
ISSN	0079-9963
ISSN	0079-9963
DOI	10.1210/rp.59.1.73
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Article ; Online: EIF3F-related neurodevelopmental disorder: refining the phenotypic and expanding the molecular spectrum.

Hüffmeier, Ulrike / Kraus, Cornelia / Reuter, Miriam S / Uebe, Steffen / Abbott, Mary-Alice / Ahmed, Syed A / Rawson, Kristyn L / Barr, Eileen / Li, Hong / Bruel, Ange-Line / Faivre, Laurence / Tran Mau-Them, Frédéric / Botti, Christina / Brooks, Susan / Burns, Kaitlyn / Ward, D Isum / Dutra-Clarke, Marina / Martinez-Agosto, Julian A / Lee, Hane /

Orphanet journal of rare diseases

2021 Volume 16, Issue 1, Page(s) 136

Abstract: Background: An identical homozygous missense variant in EIF3F, identified through a large-scale genome-wide sequencing approach, was reported as causative in nine individuals with a neurodevelopmental disorder, characterized by variable intellectual ... ...

Abstract	Background: An identical homozygous missense variant in EIF3F, identified through a large-scale genome-wide sequencing approach, was reported as causative in nine individuals with a neurodevelopmental disorder, characterized by variable intellectual disability, epilepsy, behavioral problems and sensorineural hearing-loss. To refine the phenotypic and molecular spectrum of EIF3F-related neurodevelopmental disorder, we examined independent patients. Results: 21 patients were homozygous and one compound heterozygous for c.694T>G/p.(Phe232Val) in EIF3F. Haplotype analyses in 15 families suggested that c.694T>G/p.(Phe232Val) was a founder variant. All affected individuals had developmental delays including delayed speech development. About half of the affected individuals had behavioral problems, altered muscular tone, hearing loss, and short stature. Moreover, this study suggests that microcephaly, reduced sensitivity to pain, cleft lip/palate, gastrointestinal symptoms and ophthalmological symptoms are part of the phenotypic spectrum. Minor dysmorphic features were observed, although neither the individuals' facial nor general appearance were obviously distinctive. Symptoms in the compound heterozygous individual with an additional truncating variant were at the severe end of the spectrum in regard to motor milestones, speech delay, organic problems and pre- and postnatal growth of body and head, suggesting some genotype-phenotype correlation. Conclusions: Our study refines the phenotypic and expands the molecular spectrum of EIF3F-related syndromic neurodevelopmental disorder.
MeSH term(s)	Cleft Lip ; Cleft Palate ; Eukaryotic Initiation Factor-3 ; Humans ; Intellectual Disability/genetics ; Microcephaly ; Neurodevelopmental Disorders/genetics
Chemical Substances	EIF3F protein, human ; Eukaryotic Initiation Factor-3
Language	English
Publishing date	2021-03-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-021-01744-1
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Article: Proton transport inhibitors as potentially selective anticancer drugs.

Harguindey, Salvador / Arranz, Jose Luis / Wahl, Miriam L / Orive, Gorka / Reshkin, Stephan J

Anticancer research

2009 Volume 29, Issue 6, Page(s) 2127–2136

Abstract: Different research groups have recently described a proton [H(+)]-related mechanism underlying the initiation and progression of the neoplastic process in which all cancer cells and tissues, regardless of their origin and genetic background, have a ... ...

Abstract	Different research groups have recently described a proton [H(+)]-related mechanism underlying the initiation and progression of the neoplastic process in which all cancer cells and tissues, regardless of their origin and genetic background, have a pivotal energetic and homeostatic disturbance of their metabolism that is completely different from all normal tissues: an aberrant regulation of hydrogen ion dynamics leading to a reversal of the pH gradient in cancer cells and tissues (pH(i) to pH(e)) as compared to normal tissue pH gradients. This basic specific abnormality of the relationship between the intracellular and the extracellular proton dynamics, a phenomenon that is increasingly considered to be one of the most differential hallmarks of cancer, has led to the formation of a unifying thermodynamic view of cancer research that embraces cancer fields from etiopathogenesis, cancer cell metabolism, multiple drug resistance (MDR), neovascularization and the metastatatic process to selective apoptosis, cancer chemotherapy and even the spontaneous regression of cancer (SRC). This reversed proton gradient is driven by a series of proton export mechanisms that underlie the initiation and progression of the neoplastic process. This means that therapeutic targeting of the transporters that are active in cancer cells could be selective for malignancy and is likely to open new pathways towards the development of more effective and less toxic therapeutic measures for all malignant diseases. Here we review the transporters involved in driving the reversed proton gradient and their specific inhibitors.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Humans ; Neoplasms/drug therapy ; Proton Pump Inhibitors ; Vacuolar Proton-Translocating ATPases/antagonists & inhibitors
Chemical Substances	Antineoplastic Agents ; Proton Pump Inhibitors ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
Language	English
Publishing date	2009-06
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
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Article ; Online: Brown Adipose Reporting Criteria in Imaging STudies (BARCIST 1.0): Recommendations for Standardized FDG-PET/CT Experiments in Humans.

Chen, Kong Y / Cypess, Aaron M / Laughlin, Maren R / Haft, Carol R / Hu, Houchun Harry / Bredella, Miriam A / Enerbäck, Sven / Kinahan, Paul E / Lichtenbelt, Wouter van Marken / Lin, Frank I / Sunderland, John J / Virtanen, Kirsi A / Wahl, Richard L

Cell metabolism

2016 Volume 24, Issue 2, Page(s) 210–222

Abstract: Human brown adipose tissue (BAT) presence, metabolic activity, and estimated mass are typically measured by imaging [18F]fluorodeoxyglucose (FDG) uptake in response to cold exposure in regions of the body expected to contain BAT, using positron emission ... ...

Abstract	Human brown adipose tissue (BAT) presence, metabolic activity, and estimated mass are typically measured by imaging [18F]fluorodeoxyglucose (FDG) uptake in response to cold exposure in regions of the body expected to contain BAT, using positron emission tomography combined with X-ray computed tomography (FDG-PET/CT). Efforts to describe the epidemiology and biology of human BAT are hampered by diverse experimental practices, making it difficult to directly compare results among laboratories. An expert panel was assembled by the National Institute of Diabetes and Digestive and Kidney Diseases on November 4, 2014 to discuss minimal requirements for conducting FDG-PET/CT experiments of human BAT, data analysis, and publication of results. This resulted in Brown Adipose Reporting Criteria in Imaging STudies (BARCIST 1.0). Since there are no fully validated best practices at this time, panel recommendations are meant to enhance comparability across experiments, but not to constrain experimental design or the questions that can be asked.
MeSH term(s)	Adipose Tissue, Brown/diagnostic imaging ; Fluorodeoxyglucose F18/metabolism ; Guidelines as Topic ; Humans ; Organ Size ; Positron Emission Tomography Computed Tomography ; Reproducibility of Results ; Statistics as Topic
Chemical Substances	Fluorodeoxyglucose F18 (0Z5B2CJX4D)
Language	English
Publishing date	2016-08-09
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2016.07.014
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Article ; Online: Teaching new dogs old tricks: membrane biophysical properties in drug delivery and resistance.

Milosavljevic, Nina / Blanchard, Adam / Wahl, Miriam L / Harguindey, Salvador / Poet, Mallorie / Counillon, Laurent / Rauch, Cyril

Recent patents on anti-cancer drug discovery

2011 Volume 6, Issue 3, Page(s) 334–346

Abstract: How do drugs cross the plasma membrane?" this may seem like a trivial question. This question is often overlooked to focus primarily on the different complex macro-molecular aspects involved in drug delivery or drug resistance. However, recent studies ... ...

Abstract	"How do drugs cross the plasma membrane?" this may seem like a trivial question. This question is often overlooked to focus primarily on the different complex macro-molecular aspects involved in drug delivery or drug resistance. However, recent studies have highlighted the theme that to be fully understood, more knowledge of the underlying biology of the most complex biological processes involved in the delivery and resistance to drugs is needed. After all, why would a drug interact with a transporter then subsequently be excluded from P-glycoprotein (P-gp) expressing drug resistant cells? What are the determinants of this transition in behavior? Full consideration of the physical biology of drug delivery has allowed a better understanding of the reasons why specific membrane proteins are upregulated or overexpressed in drug resistant cells. This, in turn, allows us to identify new targets for drug chemicals. Better yet, it increases the significance of recents patents and underlines their importance in multi drug resistance.
MeSH term(s)	Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacokinetics ; Biophysics ; Cell Membrane/metabolism ; Cell Membrane/physiology ; Dogs ; Drug Delivery Systems/methods ; Drug Resistance, Multiple/physiology ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/physiology ; Humans ; Models, Biological ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Surface Properties ; Wit and Humor as Topic
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2011-09
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	2250820-X
ISSN	2212-3970 ; 1574-8928
ISSN (online)	2212-3970
ISSN	1574-8928
DOI	10.2174/157489211796957829
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Article: Angiostatin induces intracellular acidosis and anoikis in endothelial cells at a tumor-like low pH.

Wahl, Miriam L / Owen, Charles S / Grant, Derrick S

Endothelium : journal of endothelial cell research

2002 Volume 9, Issue 3, Page(s) 205–216

Abstract: Angiostatin inhibits angiogenesis by binding to endothelial cells (ECs) lining the vasculature of growing tumors. These cells are in a dynamic state during angiogenesis and are thus not firmly attached to the extracellular matrix. This makes them more ... ...

Abstract	Angiostatin inhibits angiogenesis by binding to endothelial cells (ECs) lining the vasculature of growing tumors. These cells are in a dynamic state during angiogenesis and are thus not firmly attached to the extracellular matrix. This makes them more vulnerable to anoikis, a process resulting in cell death initiated by or promoted by loss of attachment. Another potential source of EC vulnerability during tumor angiogenesis is that tumor extracellular pH is typically lower than in normal tissues. This presents an additional challenge to ECs in terms of maintaining ionic homeostasis. We report here that the lethality of angiostatin is significantly enhanced both by reduced matrix attachment during exposure and lowered extracellular pH (pH(e)). Another effect of angiostatin at reduced pH(e) is a decreased intracellular pH (pH(i)). These effects were observed in three model systems: aortic ring sprouts, ECs during tube formation, and ECs in a scratch/migration assay. In these three dynamic assays, angiostatin-induced cell death and intracellular acidification were clearly seen when pH(e) was reduced to 6.7. The intracellular acidification was far greater than that induced by pH(e) reduction alone. In contrast, the effect of angiostatin on pH(i) and on viability were not observed in a subconfluent monolayer in which the cells were allowed to attach to substrate for 48 h prior to exposure to angiostatin. These data suggest that low pH(e) and reduced adhesion to matrix play a role in the specificity of angiostatin for tumor neovasculature in contrast to wound healing and other normal angiogenic processes. The results also implicate roles for both pH(e) and pH(i) regulation in the mechanism of angiostatin action.
MeSH term(s)	Acidosis/metabolism ; Angiostatins ; Animals ; Anoikis/physiology ; Cells, Cultured ; Endothelium, Vascular/chemistry ; Endothelium, Vascular/drug effects ; Guanidines/metabolism ; Humans ; Hydrogen-Ion Concentration ; Intracellular Fluid/chemistry ; Neoplasms ; Peptide Fragments/pharmacology ; Plasminogen/pharmacology ; Rats ; Sulfones/metabolism
Chemical Substances	Guanidines ; Peptide Fragments ; Sulfones ; cariporide (7E3392891K) ; Angiostatins (86090-08-6) ; Plasminogen (9001-91-6)
Language	English
Publishing date	2002-10-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1230639-3
ISSN	1543-5261 ; 1062-3329
ISSN (online)	1543-5261
ISSN	1062-3329
DOI	10.1080/10623320213633
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Article ; Online: EIF3F-related neurodevelopmental disorder

Ulrike Hüffmeier / Cornelia Kraus / Miriam S. Reuter / Steffen Uebe / Mary-Alice Abbott / Syed A. Ahmed / Kristyn L. Rawson / Eileen Barr / Hong Li / Ange-Line Bruel / Laurence Faivre / Frédéric Tran Mau-Them / Christina Botti / Susan Brooks / Kaitlyn Burns / D. Isum Ward / Marina Dutra-Clarke / Julian A. Martinez-Agosto / Hane Lee /

Orphanet Journal of Rare Diseases, Vol 16, Iss 1, Pp 1-

refining the phenotypic and expanding the molecular spectrum

2021 Volume 9

Abstract: Abstract Background An identical homozygous missense variant in EIF3F, identified through a large-scale genome-wide sequencing approach, was reported as causative in nine individuals with a neurodevelopmental disorder, characterized by variable ... ...

Abstract	Abstract Background An identical homozygous missense variant in EIF3F, identified through a large-scale genome-wide sequencing approach, was reported as causative in nine individuals with a neurodevelopmental disorder, characterized by variable intellectual disability, epilepsy, behavioral problems and sensorineural hearing-loss. To refine the phenotypic and molecular spectrum of EIF3F-related neurodevelopmental disorder, we examined independent patients. Results 21 patients were homozygous and one compound heterozygous for c.694T>G/p.(Phe232Val) in EIF3F. Haplotype analyses in 15 families suggested that c.694T>G/p.(Phe232Val) was a founder variant. All affected individuals had developmental delays including delayed speech development. About half of the affected individuals had behavioral problems, altered muscular tone, hearing loss, and short stature. Moreover, this study suggests that microcephaly, reduced sensitivity to pain, cleft lip/palate, gastrointestinal symptoms and ophthalmological symptoms are part of the phenotypic spectrum. Minor dysmorphic features were observed, although neither the individuals’ facial nor general appearance were obviously distinctive. Symptoms in the compound heterozygous individual with an additional truncating variant were at the severe end of the spectrum in regard to motor milestones, speech delay, organic problems and pre- and postnatal growth of body and head, suggesting some genotype–phenotype correlation. Conclusions Our study refines the phenotypic and expands the molecular spectrum of EIF3F-related syndromic neurodevelopmental disorder.
Keywords	EIF3F gene ; Neurodevelopmental disorder ; Short stature ; Deafness ; Behavioral difficulties ; Altered muscular tone ; Medicine ; R
Subject code	150
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: The mechanism of action of angiostatin: can you teach an old dog new tricks?

Moser, Tammy L / Stack, M Sharon / Wahl, Miriam L / Pizzo, Salvatore V

Thrombosis and haemostasis

2002 Volume 87, Issue 3, Page(s) 394–401

Abstract: What is angiostatin? In 1994, Folkman and colleagues published a landmark paper describing anti-tumor effects in mice with a purified fragment of plasminogen they named angiostatin (1). Although many papers have been published describing activities of ... ...

Abstract	What is angiostatin? In 1994, Folkman and colleagues published a landmark paper describing anti-tumor effects in mice with a purified fragment of plasminogen they named angiostatin (1). Although many papers have been published describing activities of cryptic polypeptides derived from plasminogen fragments, this was the first report which associated plasminogen kringles 1-4 as a suppressor of metastasis development. This review will describe what is known about the mechanism of action of angiostatin from the current literature.
MeSH term(s)	Angiogenesis Inhibitors/chemistry ; Angiogenesis Inhibitors/pharmacology ; Angiostatins ; Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Binding Sites ; Humans ; Mitochondrial Proton-Translocating ATPases/antagonists & inhibitors ; Peptide Fragments/chemistry ; Peptide Fragments/pharmacology ; Peptide Fragments/physiology ; Plasminogen/chemistry ; Plasminogen/pharmacology ; Plasminogen/physiology
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents ; Peptide Fragments ; Angiostatins (86090-08-6) ; Plasminogen (9001-91-6) ; Mitochondrial Proton-Translocating ATPases (EC 3.6.3.-)
Language	English
Publishing date	2002-03
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	518294-3
ISSN	0340-6245
ISSN	0340-6245
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Article: Angiostatin's molecular mechanism: aspects of specificity and regulation elucidated.

Wahl, Miriam L / Kenan, Daniel J / Gonzalez-Gronow, Mario / Pizzo, Salvatore V

Journal of cellular biochemistry

2005 Volume 96, Issue 2, Page(s) 242–261

Abstract: Tumor growth requires the development of new vessels that sprout from pre-existing normal vessels in a process known as "angiogenesis" [Folkman (1971) N Engl J Med 285:1182-1186]. These new vessels arise from local capillaries, arteries, and veins in ... ...

Abstract	Tumor growth requires the development of new vessels that sprout from pre-existing normal vessels in a process known as "angiogenesis" [Folkman (1971) N Engl J Med 285:1182-1186]. These new vessels arise from local capillaries, arteries, and veins in response to the release of soluble growth factors from the tumor mass, enabling these tumors to grow beyond the diffusion-limited size of approximately 2 mm diameter. Angiostatin, a naturally occurring inhibitor of angiogenesis, was discovered based on its ability to block tumor growth in vivo by inhibiting the formation of new tumor blood vessels [O'Reilly et al. (1994a) Cold Spring Harb Symp Quant Biol 59:471-482]. Angiostatin is a proteolytically derived internal fragment of plasminogen and may contain various members of the five plasminogen "kringle" domains, depending on the exact sites of proteolysis. Different forms of angiostatin have measurably different activities, suggesting that much remains to be elucidated about angiostatin biology. A number of groups have sought to identify the native cell surface binding site(s) for angiostatin, resulting in at least five different binding sites proposed for angiostatin on the surface of endothelial cells (EC). This review will consider the data supporting all of the various reported angiostatin binding sites and will focus particular attention on the angiostatin binding protein identified by our group: F(1)F(O) ATP synthase. There have been several developments in the quest to elucidate the mechanism of action of angiostatin and the regulation of its receptor. The purpose of this review is to describe the highlights of research on the mechanism of action of angiostatin, its' interaction with ATP synthase on the EC surface, modulators of its activity, and issues that should be explored in future research related to angiostatin and other anti-angiogenic agents.
MeSH term(s)	ATP Synthetase Complexes/metabolism ; Angiostatins/chemistry ; Angiostatins/genetics ; Angiostatins/metabolism ; Animals ; Annexin A2/metabolism ; Antigens/metabolism ; Humans ; Integrin alphaVbeta3/metabolism ; Membrane Proteins/metabolism ; Proteoglycans/metabolism
Chemical Substances	Annexin A2 ; Antigens ; Integrin alphaVbeta3 ; Membrane Proteins ; Proteoglycans ; chondroitin sulfate proteoglycan 4 ; Angiostatins (86090-08-6) ; ATP Synthetase Complexes (EC 2.7.4.-)
Language	English
Publishing date	2005-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.20480
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