Source 1review2016Viruses
Toolkit/macropinocytosis
macropinocytosis
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Macropinocytosis is a host-cell endocytic uptake route described in Kaposi’s sarcoma-associated herpesvirus (KSHV) infection models. In the cited review, KSHV enters adherent endothelial cells through membrane bleb- and actin-mediated macropinocytosis as part of broader hijacking of host signaling and membrane dynamics.
Usefulness & Problems
Why this is useful
As an engineering method, macropinocytosis provides a biologically relevant entry pathway for studying how viruses exploit host signaling, actin remodeling, and membrane dynamics during cell entry. The supplied evidence supports its usefulness specifically in adherent endothelial cell models of KSHV infection, but does not establish broader engineered applications.
Problem solved
This process helps model how KSHV gains entry into target cells through a non-clathrin, membrane bleb- and actin-dependent endocytic route. It addresses the problem of identifying cell-type-specific host entry mechanisms used during viral infection.
Problem links
Need conditional control of signaling activity
DerivedMacropinocytosis is a host-cell endocytic entry route described in KSHV infection models, in which adherent endothelial cells internalize virus through membrane bleb- and actin-mediated uptake. In the cited review, this process is presented as part of KSHV exploitation of host signaling and membrane dynamics during entry.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete method used to build, optimize, or evolve an engineered system.
Mechanisms
actin-mediated membrane remodelingactin-mediated membrane remodelingmacropinocytic uptakemacropinocytic uptakemembrane blebbingmembrane blebbingTechniques
No technique tags yet.
Target processes
signalingImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: builder
The cited context involves in vitro infection models using adherent endothelial and fibroblast cells, with macropinocytosis specifically described for adherent endothelial cells. The available evidence mentions dependence on host membrane blebbing and actin dynamics, but does not provide actionable protocol parameters, molecular perturbations, or delivery design details.
The evidence provided is limited to a review-level description of KSHV infection models and does not include primary quantitative performance data, construct details, or direct engineering demonstrations. Validation breadth is narrow because the claims are confined to specific in vitro cell models and one viral system.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
Approval Evidence
1 source2 linked approval claimsfirst-pass slug macropinocytosis
KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis
Source:
entry route by cell modelsupports
In vitro infection models described in the review use adherent endothelial and fibroblast cells, with KSHV entering by membrane bleb- and actin-mediated macropinocytosis or by clathrin endocytosis, respectively.
KSHV infection of adherent endothelial and fibroblast cells are used as in vitro models for infection and KSHV enters these cells by host membrane bleb and actin mediated macropinocytosis or clathrin endocytosis pathways, respectively.
Source:
review scope summarysupports
The review summarizes evidence that KSHV manipulates host signaling pathways to enter target cells, traffic through the cytoplasm, deliver its genome to the nucleus, and initiate viral gene expression.
This review summarizes the accumulated studies demonstrating that KSHV manipulates the host signal pathways to enter and traffic in the cytoplasm of the target cells, to deliver the viral genome into the nucleus, and initiate viral gene expression.
Source:
Comparisons
Source-backed strengths
The review explicitly distinguishes macropinocytic entry in adherent endothelial cells from clathrin endocytosis in fibroblast models, indicating cell-context-specific mechanistic resolution. It is also framed within a larger host-signaling program that supports viral entry, trafficking, nuclear delivery, and initiation of viral gene expression.
Compared with oligomerization reactions
macropinocytosis and oligomerization reactions address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
Strengths here: looks easier to implement in practice.
Compared with reversible optogenetic unmasking-masking of Ct residues
macropinocytosis and reversible optogenetic unmasking-masking of Ct residues address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
Strengths here: looks easier to implement in practice.
Compared with UVB irradiation
macropinocytosis and UVB irradiation address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
Strengths here: looks easier to implement in practice.
Ranked Citations
- 1.