On the Role of Calpain and Rho Proteins in Regulating Integrin-induced Signaling

1999 ◽  
Vol 82 (08) ◽  
pp. 385-391 ◽  
Author(s):  
Joan Fox
Keyword(s):  
Signaling Molecules ◽  
Cytoskeletal Proteins ◽  
Adherent Cells ◽  
Rho Proteins ◽  
Ligand Interactions ◽  
Platelet Aggregate ◽  
And Migration ◽  
Key Steps ◽  
A Site ◽  
Induced Changes

SummaryThe integrin family of transmembrane receptors plays an essential role in inducing the adhesion of cells to the extracellular matrix. In some cases, members of this family of receptors can bind soluble ligands or can bind receptors on other cells and, in this way, mediate interactions between cells. In all cases, once an integrin has bound, ligand signals are transmitted across the occupied integrin. These signals culminate in changes in the behavior of the cell appropriate for the adherent state of the cell. For example, in the case of platelets, an end result of the signaling induced by binding of fibrinogen to αIIbβ3 in a platelet aggregate is a reorganization of the cytoskeleton that leads to retraction of externally-bound fibrin by clots.1,2 In the case of neutrophils, cytoskeletal changes following the integrininduced interaction of neutrophils with endothelial cells lead to the migration of neutrophils into a site of injury.3,4 Other examples of the consequences of integrin-induced signaling in adherent cells include the trafficking of lymphocytes and migration of cells during development, angiogenesis, and metastasis.5-7 Numerous signaling molecules have been shown to be activated following integrin-ligand interactions.8 Many of these associate in complexes with ligand-occupied integrin and cytoskeletal proteins. However, in general, little is known about the key steps involved regarding integrin-induced changes in the behavior of adherent cells. The present chapter reviews steps involved in integrin-induced signaling, describes the evidence that calpain is one of the signaling molecules involved in this signal transduction, and discusses potential mechanisms by which cleavage of cytoskeletal proteins and signaling molecules by calpain may regulate the integrin-induced changes in cell behavior.

scholarly journals Chloroplasts at the Crossroad of Photosynthesis, Pathogen Infection and Plant Defense

2018 ◽  
Vol 19 (12) ◽  
pp. 3900 ◽  
Author(s):  
Yan Lu ◽  
Jian Yao
Keyword(s):  
Plant Defense ◽  
Defense Mechanisms ◽  
Bacterial Pathogens ◽  
Signaling Molecules ◽  
Biological Processes ◽  
Pathogen Infection ◽  
Primary Metabolites ◽  
Key Steps ◽  
A Site ◽  
Host Tissues

Photosynthesis, pathogen infection, and plant defense are three important biological processes that have been investigated separately for decades. Photosynthesis generates ATP, NADPH, and carbohydrates. These resources are utilized for the synthesis of many important compounds, such as primary metabolites, defense-related hormones abscisic acid, ethylene, jasmonic acid, and salicylic acid, and antimicrobial compounds. In plants and algae, photosynthesis and key steps in the synthesis of defense-related hormones occur in chloroplasts. In addition, chloroplasts are major generators of reactive oxygen species and nitric oxide, and a site for calcium signaling. These signaling molecules are essential to plant defense as well. All plants grown naturally are attacked by pathogens. Bacterial pathogens enter host tissues through natural openings or wounds. Upon invasion, bacterial pathogens utilize a combination of different virulence factors to suppress host defense and promote pathogenicity. On the other hand, plants have developed elaborate defense mechanisms to protect themselves from pathogen infections. This review summarizes recent discoveries on defensive roles of signaling molecules made by plants (primarily in their chloroplasts), counteracting roles of chloroplast-targeted effectors and phytotoxins elicited by bacterial pathogens, and how all these molecules crosstalk and regulate photosynthesis, pathogen infection, and plant defense, using chloroplasts as a major battlefield.

Moral navigation and child fostering in Chiawa, Zambia

Africa ◽  
2021 ◽  
Vol 91 (2) ◽  
pp. 249-269
Author(s):  
Sarah C. White ◽  
Shreya Jha
Keyword(s):  
Economic Status ◽  
Well Being ◽  
Collective Good ◽  
Geographical Proximity ◽  
Birth Parents ◽  
Social Navigation ◽  
Personal Benefit ◽  
Child Fostering ◽  
And Migration ◽  
A Site

AbstractThis article explores the movement of children between households in Zambia as a site of ‘moral navigation’. Moral navigation extends Henrik Vigh's concept of social navigation from contexts of conflict and migration to more socially stable contexts in which well-being depends critically on people's ability to manage relationships. The live, dynamic and mobile character of these relationships means that they require active, real-time cultivation and response. While having practical objectives, these negotiations are also moral, articulated with ideas of what ought to be, and seeking to fulfil sometimes competing ethical projects. Life history interviews present three main perspectives: recollections of times in childhood spent away from birth parents; birth parents’ reflections on having a child living with others; and adults’ accounts of taking in other people's children. Strong norms of kinship unity and solidarity notwithstanding, in practice terms of engagement are differentiated through gender, marital, social and economic status, plus relational and geographical proximity. The pursuit of personal benefit contains the seeds of both contradiction and convergence with the collective good, as a relational understanding of moral selves sees one's own gain as proper, rightful and virtuous when it is realized in and through providing for others.

Effect of Diamagnetic A2+ Substitution on the Magnetic and Ferroelectric Properties of the Bi1−xAxFeO3 Multiferroics

2007 ◽  
Vol 1034 ◽  
Author(s):  
V. A. Khomchenko ◽  
D. A. Kiselev ◽  
J. M. Vieira ◽  
Li Jian ◽  
A. M. L. Lopes ◽  
...  
Keyword(s):  
Spin Structure ◽  
Ionic Radius ◽  
Ferroelectric Properties ◽  
Piezoresponse Force Microscopy ◽  
Weak Ferromagnetism ◽  
Force Microscopy ◽  
Microscopy Data ◽  
A Site ◽  
Induced Changes ◽  
Spiral Spin

AbstractInvestigation of crystal structure, magnetic and local ferroelectric properties of the diamagnetically-doped Bi1−xAxFeO3 (A= Ca, Sr, Pb, Ba; x= 0.2, 0.3) ceramic samples has been carried out. It has been shown that the solid solutions have a rhombohedrally distorted perovskite structure described by the space group R3c. Piezoresponse force microscopy data have revealed the existence of the spontaneous ferroelectric polarization in the samples at room temperature. Magnetization measurements have shown that the magnetic state of these compounds is determined by the ionic radius of the substituting elements. A-site substitution with the biggest ionic radius ions has been found to suppress the spiral spin structure of BiFeO3 and to result in the appearance of weak ferromagnetism. The magnetic properties have been discussed in terms of doping- induced changes in the magnetic anisotropy.

scholarly journals Insulin induces rapid and specific rearrangement of the cytoskeleton of rat mesangial cells in vitro.

1996 ◽  
Vol 44 (2) ◽  
pp. 91-101 ◽  
Author(s):  
A K Berfield ◽  
G J Raugi ◽  
C K Abrass
Keyword(s):  
Mesangial Cells ◽  
Focal Adhesions ◽  
Cytoskeletal Proteins ◽  
Direct Effects ◽  
Ligand Effects ◽  
Igf I ◽  
Induced Changes ◽  
Secondary Ligand

Mesangial cells (MCs) grown without supplemental insulin (SI-MCs) express a quiescent phenotype and extracellular matrix (ECM) composition similar to MCs in vivo. In contrast, MCs routinely propagated in insulin (SI+MCs) are stimulated to proliferate, change their phenotype, and produce large amounts of collagens I and III. These effects of insulin may in part be mediated through cytoskeletal rearrangement. Differences in cytoskeletal arrangement were compared between SI-MCs and SI+MCs and 1 hr after addition of insulin (1 nM) or IGF-1 (100 nM) to SI-MCs. Cells were examined by light microscopy, electron microscopy, and immunostaining for specific cytoskeletal proteins and fibronectin. Insulin induced rapid rearrangement of stress fibers. Surface ruffling, actin aggregation, vimentin retraction, rearrangement of vinculin in focal adhesions, and fibronectin extraction were apparent. These direct effects of insulin on the SI-MC cytoskeleton occurred before insulin-induced changes in ECM composition. IGF-I induced cytoskeletal reorganization distinct from insulin. These observations demonstrate that insulin and IGF-I have unique effects on the MC cytoskeleton, which is turn may mediate secondary ligand effects on MCs.

Baroreflex modulation of heart rate and initiation of atrial activation in dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H503-H513 ◽  
Author(s):  
R. B. Schuessler ◽  
T. E. Canavan ◽  
J. P. Boineau ◽  
J. L. Cox
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Right Atrial ◽  
Autonomic Blockade ◽  
Left And Right ◽  
Atrial Activation ◽  
The Right ◽  
A Site ◽  
Induced Changes ◽  
Cardiac Nerves

In open-chest dogs, blood pressure was regulated by titrating doses of phenylephrine and nitroprusside to determine its effect on heart rate and pacemaker location. Changes in blood pressure correlated with changes in heart rate (r = 0.86). Activation time mapping demonstrated multicentric atrial activation, with a site of origin-rate relationship. The fastest pacemakers were located in the most cranial regions and slowest in the most caudal areas. In this chloralose-morphine anesthetized model, autonomic blockade with atropine and propranolol suggests that acute baroreflex-induced changes in heart rate were mediated exclusively by either increased sympathetic or parasympathetic tone and were not associated with inhibition of the opposite system. Division of right and left thoracic cardiac nerves indicated the left sympathetics participated in the baroreflex in 50% of the animals and the left parasympathetics in 90% of the animals. Both the right sympathetics and parasympathetics were active in the baroreflex in all animals. The data demonstrate that physiological heart rate response is regulated through an extensive system of right atrial pacemakers modulated by both left and right efferent cardiac nerves.

scholarly journals Characterization of the Roles of Vimentin in Regulating the Proliferation and Migration of HSCs during Hepatic Fibrogenesis

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1184 ◽  
Author(s):  
Pei-Wen Wang ◽  
Tung-Ho Wu ◽  
Tung-Yi Lin ◽  
Mu-Hong Chen ◽  
Chau-Ting Yeh ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Messenger Rna ◽  
Rho Gtpase ◽  
Focal Adhesions ◽  
Cytoskeletal Proteins ◽  
Nuclear Antigen ◽  
Dependent Manner ◽  
Hepatic Fibrogenesis ◽  
And Migration ◽  
Proliferation And Migration

The activation of hepatic stellate cells (HSCs) manifested as proliferation and migration is the pivotal event involved in liver fibrogenesis. The vimentin network, an intermediate filament (IF) system, is one of the critical cascades by which the cell morphology, growth, and motility are modulated. However, the vimentin-mediated cytoskeletal cross talk, as well as the signaling transduction, which further coordinates the cellular responses during hepatic fibrogenesis, is poorly understood. In the current study, both messenger RNA (mRNA) and the vimentin protein were significantly increased in a time-dependent manner in the dimethylnitrosamine (DMN)-exposed liver. In particular, vimentin was highly expressed in the activated HSCs. Again, the overexpressed vimentin was observed in the plasma samples derived from patients with hepatic fibrosis/cirrhosis, suggesting that vimentin may be a key factor in regulating the progression of liver fibrosis. Meanwhile, vimentin knockdown suppressed the migratory propensity, provoked morphological changes, and disturbed the focal adhesions in the HSCs due to the breakdown of associated cytoskeletal proteins. Western blotting showed that vimentin deletion inhibited proliferating cell nuclear antigen (PCNA) and arrested the Rho GTPase family, thereby impairing the HSCs’ growth as well as motility. The phosphorylated extracellular-signal regulated kinase (ERK) and AKT signals were also notably reduced in response to the silence of vimentin. Inhibitors of selected signaling pathways suppressed the migration and differentiation of activated HSCs by regulating specific serine phosphorylated sites on vimentin. Taken together, these findings revealed a novel mechanism of vimentin through which various signaling pathways controlled the proliferation, differentiation, and movement of the HSCs via the ERK/AKT and Rho cascades.

scholarly journals Planar Cell Polarity Acts Through Septins to Control Collective Cell Movement and Ciliogenesis

Science ◽  
2010 ◽  
Vol 329 (5997) ◽  
pp. 1337-1340 ◽  
Author(s):  
Su Kyoung Kim ◽  
Asako Shindo ◽  
Tae Joo Park ◽  
Edwin C. Oh ◽  
Srimoyee Ghosh ◽  
...  
Keyword(s):  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Control Point ◽  
Cell Movement ◽  
Cytoskeletal Proteins ◽  
Pcp Signaling ◽  
Cellular Machinery ◽  
And Migration ◽  
Controlling Behaviors ◽  
Shed Light

The planar cell polarity (PCP) signaling pathway governs collective cell movements during vertebrate embryogenesis, and certain PCP proteins are also implicated in the assembly of cilia. The septins are cytoskeletal proteins controlling behaviors such as cell division and migration. Here, we identified control of septin localization by the PCP protein Fritz as a crucial control point for both collective cell movement and ciliogenesis in Xenopus embryos. We also linked mutations in human Fritz to Bardet-Biedl and Meckel-Gruber syndromes, a notable link given that other genes mutated in these syndromes also influence collective cell movement and ciliogenesis. These findings shed light on the mechanisms by which fundamental cellular machinery, such as the cytoskeleton, is regulated during embryonic development and human disease.

scholarly journals Dissection of PIM serine/threonine kinases in FLT3-ITD–induced leukemogenesis reveals PIM1 as regulator of CXCL12–CXCR4-mediated homing and migration

2009 ◽  
Vol 206 (9) ◽  
pp. 1957-1970 ◽  
Author(s):  
Rebekka Grundler ◽  
Laurent Brault ◽  
Christelle Gasser ◽  
Alex N. Bullock ◽  
Tobias Dechow ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Surface Expression ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Antitumor Effects ◽  
Cxcr4 Signaling ◽  
Threonine Kinases ◽  
And Migration ◽  
A Site

FLT3-ITD–mediated leukemogenesis is associated with increased expression of oncogenic PIM serine/threonine kinases. To dissect their role in FLT3-ITD–mediated transformation, we performed bone marrow reconstitution assays. Unexpectedly, FLT3-ITD cells deficient for PIM1 failed to reconstitute lethally irradiated recipients, whereas lack of PIM2 induction did not interfere with FLT3-ITD–induced disease. PIM1-deficient bone marrow showed defects in homing and migration and displayed decreased surface CXCR4 expression and impaired CXCL12–CXCR4 signaling. Through small interfering RNA–mediated knockdown, chemical inhibition, expression of a dominant-negative mutant, and/or reexpression in knockout cells, we found PIM1 activity to be essential for proper CXCR4 surface expression and migration of cells toward a CXCL12 gradient. Purified PIM1 led to the phosphorylation of serine 339 in the CXCR4 intracellular domain in vitro, a site known to be essential for normal receptor recycling. In primary leukemic blasts, high levels of surface CXCR4 were associated with increased PIM1 expression, and this could be significantly reduced by a small molecule PIM inhibitor in some patients. Our data suggest that PIM1 activity is important for homing and migration of hematopoietic cells through modification of CXCR4. Because CXCR4 also regulates homing and maintenance of cancer stem cells, PIM1 inhibitors may exert their antitumor effects in part by interfering with interactions with the microenvironment.

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