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Article ; Online: MASLD/MetALD and mortality in individuals with any cardio-metabolic risk factor: a population based study with 26.7 years of follow-up.

Kwak, Minsun / Kim, Hyun-Seok / Jiang, Zhenghui Gordon / Yeo, Yee Hui / Trivedi, Hirsh D / Noureddin, Mazen / Yang, Ju Dong

Hepatology (Baltimore, Md.)

2024

Abstract: Background aims: A new term, metabolic dysfunction-associated steatotic liver disease(MASLD), has been proposed by a multi-society expert panel. However, it remains unclear whether hepatic steatosis per se in MASLD contributes to an increased risk of ... ...

Abstract	Background aims: A new term, metabolic dysfunction-associated steatotic liver disease(MASLD), has been proposed by a multi-society expert panel. However, it remains unclear whether hepatic steatosis per se in MASLD contributes to an increased risk of mortality in individuals with any cardio-metabolic risk factor(CMRF), which are also significant risk factors for increased mortality. This study aimed to compare all-cause and cause-specific mortality between the 'MASLD/MetALD' and 'no steatotic liver disease(SLD)' groups in individuals with any CMRF. Approach and results: A population-based cohort study was conducted using 10,750 participants of NHANES III. All-cause and cause-specific(cardiovascular, cancer, diabetes, and liver) mortality risks were compared between the 'MASLD', 'MetALD', and 'no SLD' groups using the Cox proportional hazards model with complex survey design weights, adjusted for confounders. Over 26 years, the 'MASLD' group did not show significantly increased all-cause(adjusted hazard ratio 1.04[95% confidence interval 0.95-1.14], p=0.413), cardiovascular(0.88[0.75-1.04], p=0.139), or cancer(1.06[0.84-1.33], p=0.635) mortality risk compared to the 'no SLD' group in individuals with any CMRF. The MetALD group was associated with increased all-cause(1.41 [1.05-1.89], p=0.022), cancer(2.35[1.33-4.16], p=0.004) and liver(15.04[2.96-76.35], p=0.002) mortality risk compared with the no SLD group. This trend was more pronounced in MetALD group with advanced fibrosis assessed by FIB-4. Conclusion: In individuals with CMRF, the presence of steatotic liver disease (MASLD) alone did not increase the risk of mortality, except in cases with more alcohol consumption (MetALD). Therefore controlling metabolic risk factors and reducing alcohol consumption in people with MASLD or MetALD will be crucial steps to improve long-term health outcomes.
Language	English
Publishing date	2024-05-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1097/HEP.0000000000000925
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Zs.A 1660: Show issues

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Article ; Online: Lipoprotein metabolism in liver diseases.

Perez-Matos, Maria Camila / Sandhu, Bynvant / Bonder, Alan / Jiang, Zhenghui Gordon

Current opinion in lipidology

2019 Volume 30, Issue 1, Page(s) 30–36

Abstract: Purpose of review: The liver is the central hub of lipoprotein metabolism. A complex relationship exists between dyslipidemia and chronic liver diseases (CLDs). Recent advances in the genetics of nonalcoholic fatty liver disease (NAFLD) and alcoholic ... ...

Abstract	Purpose of review: The liver is the central hub of lipoprotein metabolism. A complex relationship exists between dyslipidemia and chronic liver diseases (CLDs). Recent advances in the genetics of nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) exemplify the pivotal role of lipoprotein metabolism in the pathogenesis of CLD. We review these relationships in four quintessential forms of CLD: NAFLD, ALD, cholestatic liver disease and cirrhosis, with a focus on recent discoveries. Recent findings: An I148 M variant in patatin-like phospholipase domain-containing protein 3 (PNPLA3) and an E167K variant in transmembrane 6 superfamily 2 (TM6SF2) are major genetic risk factors for the development and progression of NAFLD. These genetic variants also increase the risk of ALD. Both PNPLA3 and TM6SF2 are involved in the hepatic assembly of very low-density lipoprotein. The discovery of these two genetic variants highlights the risk of CLD when environmental factors are combined with functional modifications in the lipoprotein metabolism pathway. Summary: The relationship between CLD and lipoprotein metabolism is reciprocal. On the one hand, the progression of CLD impairs lipoprotein metabolism; on the other hand, modifications in lipoprotein metabolism can substantially increase the risk of CLD. These relationships are at play among the most common forms of CLD affecting a significant proportion of the population.
MeSH term(s)	Animals ; Humans ; Lipoproteins/metabolism ; Liver Diseases/metabolism
Chemical Substances	Lipoproteins
Language	English
Publishing date	2019-02-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1045394-5
ISSN	1473-6535 ; 0957-9672
ISSN (online)	1473-6535
ISSN	0957-9672
DOI	10.1097/MOL.0000000000000569
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Article ; Online: Elevated Plasma Levels of Ketone Bodies Are Associated With All-Cause Mortality and Incidence of Heart Failure in Older Adults: The CHS.

Niezen, Sebastian / Connelly, Margery A / Hirsch, Calvin / Kizer, Jorge R / Benitez, Maria E / Minchenberg, Scott / Perez-Matos, Maria Camila / Jiang, Zhenghui Gordon / Mukamal, Kenneth J

Journal of the American Heart Association

2023 Volume 12, Issue 17, Page(s) e029960

Abstract: Background Chronic disease, such as heart failure, influences cellular metabolism and shapes circulating metabolites. The relationships between key energy metabolites and chronic diseases in aging are not well understood. This study aims to determine the ...

Abstract	Background Chronic disease, such as heart failure, influences cellular metabolism and shapes circulating metabolites. The relationships between key energy metabolites and chronic diseases in aging are not well understood. This study aims to determine the relationship between main components of energy metabolism with all-cause mortality and incident heart failure. Methods and Results We analyzed the association between plasma metabolite levels with all-cause mortality and incident heart failure among US older adults in the CHS (Cardiovascular Health Study). We followed 1758 participants without heart failure at baseline with hazard ratios (HRs) of analyte levels and metabolic profiles characterized by high levels of ketone bodies for all-cause mortality and incident heart failure. Multivariable Cox analyses revealed a dose-response relationship of 50% increase in all-cause mortality between lowest and highest quintiles of ketone body concentrations (HR, 1.5 [95% CI, 1.0-1.9];
MeSH term(s)	Humans ; Aged ; Incidence ; Heart Failure/diagnosis ; Heart Failure/epidemiology ; Cardiovascular Diseases ; Aging ; Ketone Bodies
Chemical Substances	Ketone Bodies
Language	English
Publishing date	2023-08-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.123.029960
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Article ; Online: Purinergic signaling during intestinal inflammation.

Longhi, Maria Serena / Moss, Alan / Jiang, Zhenghui Gordon / Robson, Simon C

Journal of molecular medicine (Berlin, Germany)

2017 Volume 95, Issue 9, Page(s) 915–925

Abstract: Inflammatory bowel disease (IBD) is a devastating disease that is associated with excessive inflammation in the intestinal tract in genetically susceptible individuals and potentially triggered by microbial dysbiosis. This illness markedly predisposes ... ...

Abstract	Inflammatory bowel disease (IBD) is a devastating disease that is associated with excessive inflammation in the intestinal tract in genetically susceptible individuals and potentially triggered by microbial dysbiosis. This illness markedly predisposes patients to thrombophilia and chronic debility as well as bowel, lymphatic, and liver cancers. Development of new therapies is needed to re-establish long-term immune tolerance in IBD patients without increasing the risk of opportunistic infections and cancer. Aberrant purinergic signaling pathways have been implicated in disordered thromboregulation and immune dysregulation, as noted in the pathogenesis of IBD and other gastrointestinal/hepatic autoimmune diseases. Expression of CD39 on endothelial or immune cells allows for homeostatic integration of hemostasis and immunity, which are disrupted in IBD. Our focus in this review is on novel aspects of the functions of CD39 and related NTPDases in IBD. Regulated CD39 activity allows for scavenging of extracellular nucleotides, the maintenance of P2-receptor integrity and coordination of adenosinergic signaling responses. CD39 together with CD73, serves as an integral component of the immunosuppressive machinery of dendritic cells, myeloid cells, T and B cells. Genetic inheritance and environental factors closely regulate the levels of expression and phosphohydrolytic activity of CD39, both on immune cells and released microparticles. Purinergic mechanisms associated with T regulatory and supressor T helper type 17 cells modulate disease activity in IBD, as can be modeled in experimental colitis. As a recent example, upregulation of CD39 is dependent upon ligation of the aryl hydrocarbon receptor (AHR), as with natural ligands such as bilirubin and 2-(1' H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). Decreased expression of CD39 and/or dysfunctional AHR signaling, however, abrogates the protective effects of immunosuppressive AHR ligands. These factors could also serve as biomarkers of disease activity in IBD. Heightened thrombosis, inflammation, and immune disturbances as seen in IBD appear to be associated with aberrant purinergic signaling. Ongoing development of therapeutic strategies augmenting CD39 ectonucleotidase bioactivity via cytokines or AHR ligands offers promise for management of thrombophilia, disordered inflammation, and aberrant immune reactivity in IBD.
MeSH term(s)	Adenosine/metabolism ; Animals ; Antigens, CD/metabolism ; Apyrase/metabolism ; Biomarkers ; Dysbiosis ; Exosomes/metabolism ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Inflammatory Bowel Diseases/etiology ; Inflammatory Bowel Diseases/metabolism ; Inflammatory Bowel Diseases/pathology ; Inflammatory Bowel Diseases/therapy ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Purines/metabolism ; Receptors, Aryl Hydrocarbon/metabolism ; Signal Transduction
Chemical Substances	Antigens, CD ; Biomarkers ; Hypoxia-Inducible Factor 1, alpha Subunit ; Purines ; Receptors, Aryl Hydrocarbon ; Apyrase (EC 3.6.1.5) ; CD39 antigen (EC 3.6.1.5) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2017-05-26
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-017-1545-1
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Article ; Online: Selective deletion of ENTPD1/CD39 in macrophages exacerbates biliary fibrosis in a mouse model of sclerosing cholangitis.

Rothweiler, Sonja / Feldbrügge, Linda / Jiang, Zhenghui Gordon / Csizmadia, Eva / Longhi, Maria Serena / Vaid, Kahini / Enjyoji, Keiichi / Popov, Yury V / Robson, Simon C

Purinergic signalling

2019 Volume 15, Issue 3, Page(s) 375–385

Abstract: Purinergic signaling is important in the activation and differentiation of macrophages, which play divergent roles in the pathophysiology of liver fibrosis. The ectonucleotidase CD39 is known to modulate the immunoregulatory phenotype of macrophages, but ...

Abstract	Purinergic signaling is important in the activation and differentiation of macrophages, which play divergent roles in the pathophysiology of liver fibrosis. The ectonucleotidase CD39 is known to modulate the immunoregulatory phenotype of macrophages, but whether this specifically impacts cholestatic liver injury is unknown. Here, we investigated the role of macrophage-expressed CD39 on the development of biliary injury and fibrosis in a mouse model of sclerosing cholangitis. Myeloid-specific CD39-deficient mice (LysMCreCd39
MeSH term(s)	Animals ; Antigens, CD/metabolism ; Apyrase/metabolism ; Cholangitis, Sclerosing/chemically induced ; Cholangitis, Sclerosing/metabolism ; Cholangitis, Sclerosing/pathology ; Disease Models, Animal ; Liver Cirrhosis/metabolism ; Macrophages ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pyridines/toxicity
Chemical Substances	3,5-diethoxycarbonyl-1,4-dihydrocollidine ; Antigens, CD ; Pyridines ; Apyrase (EC 3.6.1.5) ; CD39 antigen (EC 3.6.1.5)
Language	English
Publishing date	2019-06-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2172143-9
ISSN	1573-9546 ; 1573-9538
ISSN (online)	1573-9546
ISSN	1573-9538
DOI	10.1007/s11302-019-09664-3
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Article: Lipoprotein metabolism in nonalcoholic fatty liver disease.

Jiang, Zhenghui Gordon / Robson, Simon C / Yao, Zemin

Journal of biomedical research

2012 Volume 27, Issue 1, Page(s) 1–13

Abstract: Nonalcoholic fatty liver disease (NAFLD), an escalating health problem worldwide, covers a spectrum of pathologies characterized by fatty accumulation in hepatocytes in early stages, with potential progression to liver inflammation, fibrosis, and failure. ...

Abstract	Nonalcoholic fatty liver disease (NAFLD), an escalating health problem worldwide, covers a spectrum of pathologies characterized by fatty accumulation in hepatocytes in early stages, with potential progression to liver inflammation, fibrosis, and failure. A close, yet poorly understood link exists between NAFLD and dyslipidemia, a constellation of abnormalities in plasma lipoproteins including triglyceride-rich very low density lipoproteins. Apolipoproteins are a group of primarily liver-derived proteins found in serum lipoproteins; they not only play an extracellular role in lipid transport between vital organs through circulation, but also play an important intracellular role in hepatic lipoprotein assembly and secretion. The liver functions as the central hub for lipoprotein metabolism, as it dictates lipoprotein production and to a significant extent modulates lipoprotein clearance. Lipoprotein metabolism is an integral component of hepatocellular lipid homeostasis and is implicated in the pathogenesis, potential diagnosis, and treatment of NAFLD.
Language	English
Publishing date	2012-12-01
Publishing country	China
Document type	Journal Article
ZDB-ID	2555537-6
ISSN	1876-4819 ; 1674-8301
ISSN (online)	1876-4819
ISSN	1674-8301
DOI	10.7555/JBR.27.20120077
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Article ; Online: A Standardized Assessment of Functional Disability Predicts 1-year Mortality in Patients Undergoing Transjugular Intrahepatic Portosystemic Shunt for Refractory Ascites.

Grunwald, Douglas / Tapper, Elliot B / Jiang, Zhenghui Gordon / Ahmed, Muneeb / Malik, Raza

Journal of clinical gastroenterology

2016 Volume 50, Issue 1, Page(s) 75–79

Abstract: Goals: To determine the association between functional disability and mortality after transjugular intrahepatic portosystemic shunt (TIPS).: Background: TIPS is a common therapeutic procedure for cirrhotic patients with refractory ascites. The ... ...

Abstract	Goals: To determine the association between functional disability and mortality after transjugular intrahepatic portosystemic shunt (TIPS). Background: TIPS is a common therapeutic procedure for cirrhotic patients with refractory ascites. The conventional metric for periprocedure risk stratification is the model for end-stage liver disease (MELD), which uses biochemical parameters to predict post-TIPS mortality. It does not account for functional disability. Study: This is a retrospective cohort study of 83 patients admitted at an academic liver transplant center with cirrhosis and refractory ascites for the purpose of TIPS placement. We assessed the association of patients' reported activities of daily living (ADL) on a scale of 1 to 21 before TIPS with a primary outcome of 1-year mortality. Multivariable regression to adjust for MELD and Child class was performed. Results: A higher ADL score or functional independence, was associated with decreased 1-year mortality when modeled as both a continuous variable [odds ratio (OR), 0.80; 95% confidence interval (CI), 0.66-0.97; P=0.02) and a dichotomous variable (ADL 21 vs. <21; OR, 0.21; 95% CI, 0.05-0.70; P=0.01). After adjusting for MELD and Child class, functional independence was associated with decreased 1-year transplant-free mortality (OR, 0.22; 95% CI, 0.05-0.77; P=0.02). An ADL score consistent with dependence (<21) was significantly associated with a 3.40-day (95% CI, 1.76-5.04) longer hospital stay, adjusting for MELD and Child class (P<0.0001). Conclusions: Functional disability is a predictor of post-TIPS mortality and length of stay after controlling for MELD.
MeSH term(s)	Activities of Daily Living ; Ascites/mortality ; Ascites/surgery ; Cohort Studies ; Disability Evaluation ; Female ; Follow-Up Studies ; Hospitalization/statistics & numerical data ; Humans ; Length of Stay ; Liver Cirrhosis/mortality ; Liver Cirrhosis/surgery ; Male ; Middle Aged ; Multivariate Analysis ; Portasystemic Shunt, Transjugular Intrahepatic/methods ; Regression Analysis ; Retrospective Studies
Language	English
Publishing date	2016-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	448460-5
ISSN	1539-2031 ; 0192-0790
ISSN (online)	1539-2031
ISSN	0192-0790
DOI	10.1097/MCG.0000000000000339
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Zs.A 1523: Show issues

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Article ; Online: Low LDL-C and high HDL-C levels are associated with elevated serum transaminases amongst adults in the United States: a cross-sectional study.

Jiang, Zhenghui Gordon / Mukamal, Kenneth / Tapper, Elliot / Robson, Simon C / Tsugawa, Yusuke

PloS one

2014 Volume 9, Issue 1, Page(s) e85366

Abstract: Background: Dyslipidemia, typically recognized as high serum triglyceride, high low-density lipoprotein cholesterol (LDL-C) or low high-density lipoprotein cholesterol (HDL-C) levels, are associated with nonalcoholic fatty liver disease (NAFLD). However, ...

Abstract	Background: Dyslipidemia, typically recognized as high serum triglyceride, high low-density lipoprotein cholesterol (LDL-C) or low high-density lipoprotein cholesterol (HDL-C) levels, are associated with nonalcoholic fatty liver disease (NAFLD). However, low LDL-C levels could result from defects in lipoprotein metabolism or impaired liver synthetic function, and may serve as ab initio markers for unrecognized liver diseases. Whether such relationships exist in the general population has not been investigated. We hypothesized that despite common conception that low LDL-C is desirable, it might be associated with elevated liver enzymes due to metabolic liver diseases. Methods and findings: We examined the associations between alanine aminotransferase (ALT), aspartate aminotransferase (AST) and major components of serum lipid profiles in a nationally representative sample of 23,073 individuals, who had no chronic viral hepatitis and were not taking lipid-lowering medications, from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010. ALT and AST exhibited non-linear U-shaped associations with LDL-C and HDL-C, but not with triglyceride. After adjusting for potential confounders, individuals with LDL-C less than 40 and 41-70 mg/dL were associated with 4.2 (95% CI 1.5-11.7, p = 0.007) and 1.6 (95% CI 1.1-2.5, p = 0.03) times higher odds of abnormal liver enzymes respectively, when compared with those with LDL-C values 71-100 mg/dL (reference group). Surprisingly, those with HDL-C levels above 100 mg/dL was associated with 3.2 (95% CI 2.1-5.0, p<0.001) times higher odds of abnormal liver enzymes, compared with HDL-C values of 61-80 mg/dL. Conclusions: Both low LDL-C and high HDL-C, often viewed as desirable, were associated with significantly higher odds of elevated transaminases in the general U.S. adult population. Our findings underscore an underestimated biological link between lipoprotein metabolism and liver diseases, and raise a potential need for liver evaluation among over 10 million people with particularly low LDL-C or high HDL-C in the United States.
MeSH term(s)	Adult ; Alanine Transaminase/blood ; Aspartate Aminotransferases/blood ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Cross-Sectional Studies ; Female ; Humans ; Male ; Middle Aged ; United States
Chemical Substances	Cholesterol, HDL ; Cholesterol, LDL ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2)
Language	English
Publishing date	2014-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0085366
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Article: Limited proteolysis and biophysical characterization of the lipovitellin homology region in apolipoprotein B.

Jiang, Zhenghui Gordon / Carraway, Margaretha / McKnight, C James

Biochemistry

2005 Volume 44, Issue 4, Page(s) 1163–1173

Abstract: Apolipoprotein B (apoB) is the essential nonexchangeable protein in chylomicrons and very low-density lipoprotein-derived lipoprotein particles, including low-density lipoprotein (LDL). ApoB has been a key target for cardiovascular research because of ... ...

Abstract	Apolipoprotein B (apoB) is the essential nonexchangeable protein in chylomicrons and very low-density lipoprotein-derived lipoprotein particles, including low-density lipoprotein (LDL). ApoB has been a key target for cardiovascular research because of its essential role in the assembly, secretion, delivery, and receptor binding of LDL. The three-dimensional structure of apoB has not been determined. However, the N-terminal region of apoB is homologous to the lipid storage protein lipovitellin, which allows the modeling of this region based on the X-ray structure of lipovitellin. The model of the N-terminal 17% of apoB (B17) suggests that, like lipovitellin, B17 consists of an N-terminal beta-barrel domain, a helical domain, and a beta-sheet domain (C-sheet). Here we test the validity of this model by limited proteolysis of B17 and the characterization of individual domains expressed in Escherichia coli and insect cell systems that are consistent with the model and proteolysis data. Circular dichroism studies of the individual domains indicate that they are folded and their secondary structures are in agreement with the model. We find that the helical domain and C-sheet of apoB interact with each other in vitro, suggesting a strong interaction between these two domains, even without a covalent peptide bond linkage. Our data suggest that the three lipovitellin-like domains exist in B17. Furthermore, the domains fold independently with secondary structures and stabilities like those of intact B17.
MeSH term(s)	Animals ; Apolipoproteins B/genetics ; Apolipoproteins B/isolation & purification ; Apolipoproteins B/metabolism ; Biophysics/methods ; Circular Dichroism ; Cross-Linking Reagents/chemistry ; Cross-Linking Reagents/metabolism ; Egg Proteins ; Egg Proteins, Dietary/isolation & purification ; Egg Proteins, Dietary/metabolism ; Hydrolysis ; Models, Molecular ; Peptide Fragments/genetics ; Peptide Fragments/isolation & purification ; Peptide Fragments/metabolism ; Protein Folding ; Protein Structure, Secondary/genetics ; Protein Structure, Tertiary/genetics ; Sequence Homology, Amino Acid ; Spodoptera/genetics ; Trypsin/metabolism
Chemical Substances	Apolipoproteins B ; Cross-Linking Reagents ; Egg Proteins ; Egg Proteins, Dietary ; Peptide Fragments ; lipovitellin (9088-43-1) ; Trypsin (EC 3.4.21.4)
Language	English
Publishing date	2005-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Validation Studies
ZDB-ID	1108-3
ISSN	1520-4995 ; 0006-2960
ISSN (online)	1520-4995
ISSN	0006-2960
DOI	10.1021/bi048286y
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Article: A phosphorylation-induced conformation change in dematin headpiece.

Jiang, Zhenghui Gordon / McKnight, C James

Structure (London, England : 1993)

2005 Volume 14, Issue 2, Page(s) 379–387

Abstract: Dematin is an actin binding protein from the junctional complex of the erythrocyte cytoskeleton. The protein has two actin binding sites and bundles actin filaments in vitro. This actin bundling activity is reversibly regulated by phosphorylation in the ... ...

Abstract	Dematin is an actin binding protein from the junctional complex of the erythrocyte cytoskeleton. The protein has two actin binding sites and bundles actin filaments in vitro. This actin bundling activity is reversibly regulated by phosphorylation in the carboxyl terminal "headpiece" domain (DHP). DHP is a typical villin-type headpiece actin binding motif and contains a flexible N-terminal loop and an alpha-helical C-terminal subdomain that is phosphorylated at Ser74. The NMR structure of a Ser74-to-Glu mutant (DHPs74e) closely mimics the conformation of phosphorylated DHP. The negative charge at Ser74 does not alter the conformation of the C-terminal subdomain, but attracts the N-terminal loop toward the C terminus, changing the orientation of the N-terminal subdomain. NMR relaxation studies also indicate reduced mobility in the N-terminal loop in DHPs74e. Thus, phosphorylation in DHP serves as a switch controlling the conformational state of DHP and the actin bundling activity of dematin.
MeSH term(s)	Blood Proteins/chemistry ; Blood Proteins/genetics ; Blood Proteins/metabolism ; Humans ; Microfilament Proteins/chemistry ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Models, Molecular ; Motion ; Mutagenesis, Site-Directed ; Nuclear Magnetic Resonance, Biomolecular ; Phosphoproteins/chemistry ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Structure, Tertiary
Chemical Substances	Blood Proteins ; DMTN protein, human ; Microfilament Proteins ; Phosphoproteins
Language	English
Publishing date	2005-12-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1213087-4
ISSN	1878-4186 ; 0969-2126
ISSN (online)	1878-4186
ISSN	0969-2126
DOI	10.1016/j.str.2005.11.007
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