scholarly journals New Proteins Found Interacting with Brain Metallothionein-3 Are Linked to Secretion

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Issam El Ghazi ◽  
Bruce L. Martin ◽  
Ian M. Armitage
Keyword(s):  
Immunoaffinity Chromatography ◽  
Glycolytic Metabolism ◽  
Interacting Protein ◽  
Aldolase C ◽  
Growth Inhibitory Factor ◽  
Protein Partners ◽  
Growth Inhibitory ◽  
Proposed Model ◽  
The Brain ◽  
Partner Proteins

Metallothionein 3 (MT-3), also known as growth inhibitory factor (GIF), exhibits a neuroinhibitory activity. Our lab and others have previously shown that this biological activity involves interacting protein partners in the brain. However, nothing specific is yet known about which of these interactions is responsible for the GIF activity. In this paper, we are reporting upon new proteins found interacting with MT-3 as determined through immunoaffinity chromatography and mass spectrometry. These new partner proteins—Exo84p, 14-3-3 Zeta,αandβEnolase, Aldolase C, Malate dehydrogenase, ATP synthase, and Pyruvate kinase—along with those previously identified have now been classified into three functional groups: transport and signaling, chaperoning and scaffolding, and glycolytic metabolism. When viewed together, these interactions support a proposed model for the regulation of the GIF activity of MT-3.

scholarly journals A Drosophila Insulator Interacting Protein Suppresses Enhancer-Blocking Function and Modulates Replication Timing

2019 ◽  
Author(s):  
Emily C. Stow ◽  
Ran An ◽  
Todd A. Schoborg ◽  
Nastasya M. Davenport ◽  
James R. Simmons ◽  
...  
Keyword(s):  
Genome Structure ◽  
Nuclear Lamina ◽  
Replication Timing ◽  
Interacting Protein ◽  
Insulator Protein ◽  
Protein Partners ◽  
Insulator Proteins ◽  
Enhancer Blocking ◽  
And Function ◽  
Partner Proteins

AbstractInsulators play important roles in genome structure and function in Drosophila and mammals. More than six different insulator proteins are required in Drosophila for normal genome function, whereas CTCF is the only identified protein contributing to insulator function in mammals. Interactions between a DNA binding insulator protein and its interacting partner proteins define the properties of each insulator site. The different roles of insulator protein partners in the Drosophila genome and how they confer functional specificity remain poorly understood. Functional analysis of insulator partner proteins in Drosophila is necessary to understand how genomes are compartmentalized and the roles that different insulators play in genome function. In Drosophila, the Suppressor of Hairy wing [Su(Hw)] insulator is targeted to the nuclear lamina, preferentially localizes at euchromatin/heterochromatin boundaries, and is associated with the Gypsy retrotransposon. The properties that the insulator confers to these sites rely on the ability of the Su(Hw) protein to bind the DNA at specific sites and interact with Mod(mdg4)-67.2 and CP190 partner proteins. HP1 and insulator partner protein 1 (HIPP1) is a recently identified partner of Su(Hw), but how HIPP1 contributes to the function of Su(Hw) insulators has not yet been elucidated. Here, we find that mutations in the HIPP1 crotonase-like domain have no impact on the function of Su(Hw) enhancer-blocking activity but do exhibit an impaired ability to repair double-strand breaks. Additionally, we find that the overexpression of each HIPP1 and Su(Hw) causes defects in cell proliferation by limiting the progression of DNA replication. We also find that HIPP1 overexpression suppresses the Su(Hw) insulator enhancer-blocking function.

Rab11 family-interacting protein 4, RAB11FIP4, is a differentially expressed gene in brain metastatic human breast cancer.

2021 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Differentially Expressed Gene ◽  
Metastatic Breast ◽  
Metastatic Tumor ◽  
Clinical Problem ◽  
Interacting Protein ◽  
Primary Tumors ◽  
Free Survival ◽  
The Brain

Metastasis to the brain is a clinical problem in patients with breast cancer (1-3). We mined published microarray data (4, 5) to compare primary and metastatic tumor transcriptomes for the discovery of genes associated with brain metastasis in humans with metastatic breast cancer. We found that Rab11 family-interacting protein 4, encoded by RAB11FIP4, was among the genes whose expression was most different in the brain metastases of patients with metastatic breast cancer as compared to primary tumors of the breast. RAB11FIP4 mRNA was present at increased quantities in brain metastatic tissues as compared to primary tumors of the breast. Importantly, expression of RAB11FIP4 in primary tumors was significantly correlated with patient recurrence-free survival and distant metastasis-free survival. Modulation of RAB11FIP4 expression may be relevant to the biology by which tumor cells metastasize from the breast to the brain in humans with metastatic breast cancer.

scholarly journals Relations between post-mortem alterations and glycolytic metabolism in the brain

1961 ◽  
Vol 4 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Reinhard L. Friede ◽  
Wiecher H. van Houten
Keyword(s):  
Post Mortem ◽  
Glycolytic Metabolism ◽  
The Brain

scholarly journals Could a Growth Inhibitory Factor, Present Only during Pregnancy, be Made Available to Treat Cancer in Adults? A Commentary

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Mizejewski GJ
Keyword(s):  
Fetal Growth ◽  
Therapeutic Agent ◽  
Germ Cell Tumors ◽  
Inhibitory Factor ◽  
Additional Function ◽  
Major Function ◽  
Growth Inhibitory Factor ◽  
Growth Inhibitory ◽  
Age Dependent ◽  
Growth Promoting

Human alpha-fetoprotein (AFP) is well-known as the “gold standard” biomarker for liver and germ cell tumors. It has also been utilized as a pregnancy screening analyte for neural tube defects as well as Down syndrome, when combined with other gestational-age dependent biomarkers. However, a lesser known and recognized property of AFP is its role in the maintenance and monitoring of fetal growth during ontogenetic development in man. Although a major function of AFP during pregnancy involves the serum transport of estrogens, fatty acids, retinoid, and other compounds, the positive and negative regulation of fetal growth is a vital additional function of AFP. Human AFP largely functions as a growth promoting agent; however, the fetal protein is able to temporarily convert to a growth inhibitory factor in stress and shock environments in the fetal milieu. The development of a transient form of AFP or its derived peptides could be harnessed for use as an adjunct therapeutic agent to treat cancer in adults.

Normal mouse lung tissue produces a growth-inhibitory factor(s) preferential for mouse monocytic leukemia cells

1989 ◽  
Vol 30 (3) ◽  
pp. 139-144 ◽  
Author(s):  
Togo Ikuta ◽  
Yoshio Honma ◽  
Junko Okabe-Kado ◽  
Takashi Kasukabe ◽  
Motoo Hozumi
Keyword(s):  
Lung Tissue ◽  
Normal Mouse ◽  
Inhibitory Factor ◽  
Leukemia Cells ◽  
Mouse Lung ◽  
Monocytic Leukemia ◽  
Growth Inhibitory Factor ◽  
Growth Inhibitory ◽  
Mouse Lung Tissue

A Model of Metabolic Supply-Demand Mismatch Leading to Secondary Brain Injury

2021 ◽  
Author(s):  
Jiangling Song ◽  
Jennifer A. Kim ◽  
Aaron Frank Struck ◽  
Rui Zhang ◽  
M. Brandon Westover
Keyword(s):  
Brain Injury ◽  
Mechanistic Model ◽  
Acute Brain Injury ◽  
Extracellular Potassium ◽  
Secondary Brain Injury ◽  
Proposed Model ◽  
The Common ◽  
High Level ◽  
The Brain ◽  
Common Association

Secondary brain injury (SBI) is defined as new or worsening injury to the brain after an initial neurologic insult, such as hemorrhage, trauma, ischemic stroke, or infection. It is a common and potentially preventable complication following many types of primary brain injury (PBI). However, mechanistic details about how PBI leads to additional brain injury and evolves into SBI are poorly characterized. In this work, we propose a mechanistic model for the metabolic supply demand mismatch hypothesis (MSDMH) of SBI. Our model, based on the Hodgkin-Huxley model, supplemented with additional dynamics for extracellular potassium, oxygen concentration and excitotoxity, provides a high-level unified explanation for why patients with acute brain injury frequently develop SBI. We investigate how decreased oxygen, increased extracellular potassium, excitotoxicity, and seizures can induce SBI, and suggest three underlying paths for how events following PBI may lead to SBI. The proposed model also helps explain several important empirical observations, including the common association of acute brain injury with seizures, the association of seizures with tissue hypoxia and so on. In contrast to current practices which assume that ischemia plays the predominant role in SBI, our model suggests that metabolic crisis involved in SBI can also be non-ischemic. Our findings offer a more comprehensive understanding of the complex interrelationship among potassium, oxygen, excitotoxicity, seizures and SBI.

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