Source 1review2016Viruses
Toolkit/clathrin endocytosis
clathrin endocytosis
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Clathrin endocytosis is a host-cell internalization pathway described in a review as one route used by Kaposi’s sarcoma-associated herpesvirus (KSHV) to enter fibroblast infection models. In this context, it serves as a cellular uptake mechanism associated with viral entry and subsequent trafficking events linked to host signaling pathways.
Usefulness & Problems
Why this is useful
This pathway is useful as a defined cellular entry route for studying how KSHV gains access to fibroblast cells in vitro. The cited review places it within a broader framework in which host signaling, intracellular trafficking, nuclear delivery, and viral gene expression are coordinated during infection.
Problem solved
It helps address the problem of how KSHV enters specific target cell models, particularly fibroblasts, where the review cites clathrin endocytosis as an entry route. The evidence does not describe it as an engineered reagent, but as a host process relevant to dissecting virus entry and signaling-associated trafficking.
Problem links
Need conditional control of signaling activity
DerivedClathrin endocytosis is a host-cell internalization pathway cited in this review as one route used by Kaposi’s sarcoma-associated herpesvirus (KSHV) to enter fibroblast infection models. In the cited context, it functions as a cellular uptake mechanism linked to viral entry and downstream signaling-related trafficking events.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete method used to build, optimize, or evolve an engineered system.
Techniques
No technique tags yet.
Target processes
signalingImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: builder
The available evidence indicates use in in vitro infection models involving adherent fibroblast cells, where KSHV enters via clathrin endocytosis. No construct design, delivery modality, cofactors, or expression-system details are provided in the supplied text.
The supplied evidence comes from a review summary rather than a primary engineering study, so tool-like performance characteristics, construct details, and quantitative benchmarks are not provided. The evidence also does not specify molecular components, perturbation methods, or whether this pathway was directly manipulated for engineering purposes.
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 clathrin-endocytosis
KSHV enters these cells by ... clathrin endocytosis pathways
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 clathrin endocytosis as the KSHV entry route in fibroblast models, contrasting it with macropinocytosis in adherent endothelial cells. This cell-type-specific framing makes it useful for mechanistic comparison of viral uptake pathways across in vitro infection systems.
Compared with macropinocytosis
clathrin endocytosis and macropinocytosis address a similar problem space because they share signaling.
Shared frame: same top-level item type; shared target processes: signaling
Compared with reversible optogenetic unmasking-masking of Ct residues
clathrin endocytosis 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
clathrin endocytosis 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.