The DOI matches its Crossref record; 68 of the 68 references it cites were found in a registry or an index; 11 of the 35 sources its claims cite were checked for support.
Disabled‐2 exhibits the properties of a cargo‐selective endocytic clathrin adaptor
Open accessAbstract
Clathrin-coated pits at the cell surface select material for transportation into the cell interior. A major mode of cargo selection at the bud site is via the micro 2 subunit of the AP-2 adaptor complex, which recognizes tyrosine-based internalization signals. Other internalization motifs and signals, including phosphorylation and ubiquitylation, also tag certain proteins for incorporation into a coated vesicle, but the mechanism of selection is unclear. Disabled-2 (Dab2) recognizes the FXNPXY internalization motif in LDL-receptor family members via an N-terminal phosphotyrosine-binding (PTB) domain. Here, we show that in addition to binding AP-2, Dab2 also binds directly to phosphoinositides and to clathrin, assembling triskelia into regular polyhedral coats. The FXNPXY motif and phosphoinositides contact different regions of the PTB domain, but can stably anchor Dab2 to the membrane surface, while the distal AP-2 and clathrin-binding determinants regulate clathrin lattice assembly. We propose that Dab2 is a typical member of a growing family of cargo-specific adaptor proteins, including beta-arrestin, AP180, epsin, HIP1 and numb, which regulate clathrin-coat assembly at the plasma membrane by synchronizing cargo selection and lattice polymerization events.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
Dab2 binds AP-2, clathrin, and phosphoinositides, and can assemble clathrin triskelia into polyhedral coats on liposome templates. The authors propose Dab2 is a cargo-selective endocytic adaptor for FXNPXY-bearing cargo such as LDL-receptor family members.
Key findings
- Dab2’s central region binds AP-2 and clathrin: residues 206–368 are minimal for optimal AP-2 binding, while residues 206–258 bind clathrin; mutation of the type I clathrin-box 236LVDLN to AAALN nearly abolishes clathrin binding in the smallest fragment, and combined LVD→AAA/W→A mutation in 206–368 reduces clathrin binding 4- to 5-fold without affecting AP-2 binding.
- Dab2 binds preassembled clathrin cages and assembles soluble clathrin trimers into sedimentable polyhedral cages; GST–Dab2(1–368) recruits clathrin, and EM shows regular polyhedral clathrin cages, whereas the minimal clathrin-binding fragment GST–Dab2(206–258) does not increase clathrin recovery above background.
- The N-terminal PTB domain (residues 1–205) binds phosphoinositides; monomeric PTB binds ~25-fold better to PtdIns(4,5)P2 liposomes, rising from ~2% without phosphoinositide to >50% bound, and can bind phosphoinositides and an LDL-receptor FXNPXY peptide simultaneously.
- In COS-7 cells, overexpression of myc-Dab2 PTBx2 selectively blocks diI-LDL uptake during a 15 min pulse while transferrin uptake remains normal; in liposome assays, AP-2 plus GST–Dab2 leads to ~50% of total clathrin assembling onto sedimenting liposomes, with ~one-quarter of liposome-bound coat components resistant to 1% Triton X-100.
Methods
- In vitro binding assays used GST–Dab2 truncations and mutants immobilized on GSH–Sepharose incubated with rat brain cytosol, followed by SDS–PAGE and immunoblotting for AP-2 subunits and clathrin heavy/light chains.
- Clathrin assembly was tested by mixing purified clathrin with GST–Dab2 fusions, differential centrifugation, negative-stain EM, and liposome/monolayer assays with mixed lipids, phosphoinositides, purified AP-2, and clathrin; Triton X-100 extraction assessed coat assembly.
- Cell assays included immunofluorescence co-localization of Dab2 and epsin 1 in HeLa cells, and COS-7 transfection with myc-tagged Dab2 PTBx2 followed by diI-LDL and transferrin uptake; siRNA knockdown of Dab2 by >90% in HeLa cells did not inhibit diI-LDL uptake (not shown).
Limitations
- The paper states no explicit limitations section. It notes that siRNA knockdown of Dab2 by >90% in HeLa cells did not inhibit diI-LDL uptake, that no mutations in Dab2 have been linked to hypercholesterolemia, and that Dab2 is not expressed ubiquitously, with many ovarian and breast carcinomas failing to express it, suggesting possible compensation by other PTB-domain proteins.
- Evident from the text: many central assembly conclusions rely on in vitro assays with purified proteins and synthetic liposomes; PTBx2 overexpression may not reflect endogenous Dab2 function; some supporting data are “not shown”; and the anti-Dab2 antibody detects all three splice isoforms (p67, p93, p96), so distinct isoform locations cannot be concluded.
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Claims the paper makes
31 Own result · 20 Own interpretation · 9 No full text of the sources · 7 Supported · 4 Not checked yet · 3 Sources not found · 2 Supported so far · 1 Partly supported · 1 No basis given · accuracy not yet measured
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Importantly, and in contrast to eps15 (Cupers et al., 1998), extensive clathrin recruitment does not disrupt the interaction between AP-2 and either Dab2 or epsin (Figure 8) (Mishra et al., 2001), AP180 (Ford et al., 2001) or HIP1 (Mishra et al., 2001), such that these proteins are now released from the membrane surface.”
What the sources say
- Not checked — no full text of the sourcecites Cupers et al., 1998 source
- Supportedcites Mishra et al., 2001 source
The Results report that HIP1 or epsin increases AP-2 recovery on liposomes while both proteins and AP-2 recruit soluble clathrin to the liposome surface. This supports the part attributed to Mishra et al.: clathrin recruitment does not disrupt AP-2 association with HIP1 or epsin. The citing sentence attributes Dab2 to its own Figure 8 and AP180 to Ford et al., not to this paper. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Ford et al., 2001 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Pre-incubating liposomes together with a mixture of AP-2 and the GST±Dab2 fusion increases the recovery of both proteins in the liposome pellet (Figure 8C, lane h), validating the AP-2±Dab2 interactions seen in pull-down assays (Figures 1 and 2) (Morris and Cooper, 2001).”
What the sources say
- Supportedcites Morris and Cooper, 2001 source
The cited paper’s Figure 7 caption (p. 121) describes GST-Dab2 pull-down assays in which bound α-adaptin (AP-2) was detected. The citation supports the earlier AP-2–Dab2 interaction invoked at the end of the citing sentence; the liposome-pellet result is presented there as the citing authors’ own Figure 8C finding. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Dab2 binds to AP-2 directly via a central portion that, like epsin, AP180 and HIP1, engages the independently folded appendage domain of the AP-2 a-subunit (Morris and Cooper, 2001).”
What the sources say
- Supportedcites Morris and Cooper, 2001 source
The paper’s in-vitro binding results (p. 116) show that Dab2 binds the carboxy-terminal ear, or appendage, domain of AP-2 α-adaptin and identify Dab2 residues 206–492 as important for the interaction. This supports the citing sentence’s attribution of the interaction to Dab2’s central portion. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Direct association of the Dab2 PTB domain with Smad2/3 has been reported (Hocevar et al., 2001).”
What the sources say
- Supportedcites Hocevar et al., 2001 source
In “The role of PTB domain-containing proteins in signal transduction,” the authors identify the MH2 domains of Smad2 and Smad3 as binding partners of the Dab2 PTB domain. The “Dab2 associates with Smad2 and Smad3” section reports that PTB-containing Dab2 constructs bind both proteins. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This links Dab2 to megalin endocytosis in the kidney in vivo.”
What the sources say
- Supportedcites Morris et al., 2002b source
The Discussion links Dab2 to megalin-dependent protein trafficking in kidney proximal tubule cells, based on fewer apical coated pits and vesicles and increased urinary excretion of proteins. The adult-kidney transport section likewise says these findings suggest reduced megalin-mediated re-uptake in conditionally null mice. This supports the stated in vivo link without implying that megalin endocytosis is completely blocked. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This distinguishes this group of proteins from b-arrestin, which, despite also containing PtdIns(4,5)P 2 -, AP-2-and clathrinbinding determinants, appears to accompany heptahelical receptors into existing coated buds (Santini et al., 2002;Scott et al., 2002).”
What the sources say
- Supportedcites Santini et al., 2002 source
The Results section (‘Arr3 is recruited to preexisting CPs upon agonist activation’; page not specified) reports that arrestin3 moved to preexisting coated pits after β2-adrenergic receptor stimulation. The Discussion likewise says activated receptor–arrestin3 complexes rapidly accumulate in preexisting pits rather than forming new ones. The paper identifies arrestin3 as β-arrestin2, so this supports the citing sentence’s qualified description of β-arrestin behavior. (LLM, conf=0.91)
- Supportedcites Scott et al., 2002 source
The Results and Discussion report that β-arrestin2 and the activated TRHR colocalize, and explicitly describe recruitment of the TRHR–β-arrestin2 complex to pre-existing clathrin-coated pits (Fig. 4). Figure 5 also shows β-arrestin moving to pre-existing pit-formation sites after receptor stimulation. (LLM, conf=0.93)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These additional functional sequences argue that, like numb (Santolini et al., 2000), Dab2 probably accompanies the clathrin-coated vesicle during budding and ®ssion.”
What the sources say
- Supportedcites Santolini et al., 2000 source
The Results and Discussion sections on Numb localization and receptor cotrafficking report Numb in clathrin-coated pits and vesicles, moving with internalizing receptors into vesicle intermediates. This supports the cited comparison to Numb; the statement about Dab2 is the citing authors’ own inference. Page numbers are not available in our copy. (LLM, conf=0.88)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Myosin VI is a component of some clathrin-coated vesicles (Buss et al., 2001) and Dab2 probably plays an important role in targeting this motor to the vesicle.”
What the sources say
- Supportedcites Buss et al., 2001 source
The citation is attached to the claim that myosin VI is a component of some clathrin-coated vesicles, not to the subsequent proposal about Dab2. The Abstract reports that myosin VI is enriched in purified clathrin-coated vesicles, supporting the cited claim. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Inoue et al., 2002 source
- Not checked — no full text of the sourcecites Morris et al., 2002a source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Dab2 PTB association with phosphoinositide-containing mixed liposomes does not preclude NPXY sequence engagement.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Approximately one-quarter of the liposome-bound coat components are resistant to extraction with 1% Triton X-100 (Figure 8C, lane j), which has been shown by others to correlate well with extensive assembly into curved polyhedral coats (Ford et al., 2001).”
What the sources say
- Not checked — no full text of the sourcecites Ford et al., 2001 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Probably not a substantial claim. 14
- It may state two separate claims as one. 12
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The CSF-1 receptor utilizes ubiquitin as an endocytic signal (Lee et al., 1999), but the NPF triplets in Dab2 could recruit eps15, which, like epsin, can bind ubiquitin directly (Polo et al., 2002).”
What the sources say
- Partly supportedcites Lee et al., 1999 sourceExperimental — accuracy not yet measured
In “Cbl-targeted CSF-1R multiubiquitination” (page unavailable), the paper reports that CSF-1R is ubiquitinated before endocytosis and suggests that multiubiquitination may promote it. It explicitly says it is unclear whether ubiquitination of Cbl, the receptor, or both is required for internalization, so it does not establish that ubiquitin on CSF-1R serves as the endocytic signal. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“AP180 could actively cluster synaptobrevin/VAMP (Nonet et al., 1999).”
What the sources say
- Supportedcites Nonet et al., 1999 source
In “AP180 and Sorting of Vesicle Proteins” (page not supplied), the authors propose that UNC-11, an AP180 homologue, may sort synaptobrevin by binding it directly or sequestering it through other proteins. That supports the citing sentence’s tentative claim that AP180 could actively cluster synaptobrevin/VAMP; the mechanism is proposed, not demonstrated. (LLM, conf=0.87)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Protein±lipid overlays reveal that the Dab2 PTB domain displays a preference for PtdIns(4,5)P 2 , although there is binding to several phosphoinositides in this type of assay (Figure 6C).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Oriented in this way upon a 10% PtdIns(4,5)P 2 -containing monolayer of mixed lipids (Ford et al., 2001), the protein is able to recruit soluble clathrin and drive the formation of regular polyhedral structures (Figure 8A and B), which, alone, does not associate with the monolayer (Figure 8A, inset, see C, lane b).”
What the sources say
- Not checked — no full text of the sourcecites Ford et al., 2001 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The in vitro assembly of clathrin cages by Dab2 on liposome templates reflects the mechanism of clathrin-coated pit assembly at the plasma membrane.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Indeed, in HeLa cells, epsin 1 and Dab2 show extensive co-localization at steady state (Figure 5), indicating that the two proteins are probably present within common clathrin-coated struc-tures.”
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PTBx2-expressing cells, unable to internalize diI-LDL during a 15 min pulse, nevertheless take up transferrin normally compared with the surrounding, untransfected cells (Figure 7E±H).”
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Surprisingly, the removal of the FXDXF motif has no discernible effect on AP-2 binding, indicating that this sequence is not critical for the a-appendage association measured by these assays.”
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we note that the intracellular distribution of Dab2 appears to alter with the cell cycle.”
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Dab2 binds to both the AP-2 adaptor complex and clathrin.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The asterisk denotes a stable ~25 kDa thrombin degradation product that binds phosphoinositides and reacts with the anti-Dab2 mAb 52.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We propose that Dab2 is a typical member of a growing family of cargo-speci®c adaptor proteins, including b-arrestin, AP180, epsin, HIP1 and numb, which regulate clathrin-coat assembly at the plasma membrane by synchronizing cargo selection and lattice polymerization events.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The behavior of GST±Dab2 closely parallels that of a GST±epsin 1(1±407) fusion in these assays (Figure 8C, lanes k±n), showing that Dab2 can function analogously to known endocytic accessory proteins (Chen et al., 1998;Yamabhai et al., 1998;Drake et al., 2000;Mishra et al., 2001).”
What the sources say
- Not checked — no full text of the sourcecites Chen et al., 1998 source
- Not checked yetcites Yamabhai et al., 1998 source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites Drake et al., 2000 source
Checked before — its earlier verdict is held back until a new check runs.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As little AP-2 binds to the GST±Dab2 (206±258) protein (lanes d), the interaction with clathrin is largely independent of the adaptor complex and may well be direct.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A potential cargo for HIP1 is huntingtin, which interacts with the N-terminal segment of HIP1 (Wanker et al., 1997) and has been localized to clathrin-coated structures and endosomes (Velier et al., 1998).”
What the sources say
- Not checked — no full text of the sourcecites Velier et al., 1998 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“A potential cargo for HIP1 is huntingtin, which interacts with the N-terminal segment of HIP1 (Wanker et al., 1997) and has been localized to clathrin-coated structures and endosomes (Velier et al., 1998).”
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Epsin might be part of the long-sought-after machinery that recognizes ubiquitin as an endocytic signal (Polo et al., 2002).”
What the sources say
- Not checked — no full text of the sourcecites Polo et al., 2002 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“A potential cargo for HIP1 is huntingtin, which interacts with the N-terminal segment of HIP1 (Wanker et al., 1997) and has been localized to clathrin-coated structures and endosomes (Velier et al., 1998).”
What the sources say
- Not checked — no full text of the sourcecites Wanker et al., 1997 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These multifaceted connections may be a critical aspect of ensuring the ®delity of cargo incorporation into assembling coated buds.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
In the paper
“The protein was initially identi®ed as a prominent phosphoprotein accompanying colony-stimulating factor-1 (CSF-1) receptor activation (Xu et al., 1995).”
What the sources say
- Not matchedcites Xu et al., 1995
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“The CSF-1 receptor utilizes ubiquitin as an endocytic signal (Lee et al., 1999), but the NPF triplets in Dab2 could recruit eps15, which, like epsin, can bind ubiquitin directly (Polo et al., 2002).”
What the sources say
- Not checked — no full text of the sourcecites Polo et al., 2002 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Mammalian EH domain-containing proteins include eps15, intersectin, POB-1 and EHD1 (Santolini et al., 1999).”
What the sources say
- Not checked — no full text of the sourcecites Santolini et al., 1999 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This suggests that other PTB domain proteins might compensate or substitute for Dab2 loss, and thus Dab2 would not be singularly responsible for LDL receptor incorporation into clathrincoated vesicles.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Dab2 is also implicated in transforming growth factor b (TGF-b) receptor activation and downstream Smad activation (Hocevar et al., 2001).”
What the sources say
- Not checked yetcites Hocevar et al., 2001 source
Checked before — its earlier verdict is held back until a new check runs.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Rather, like epsin and AP180, it potentiates AP-2-driven coat formation, perhaps also determining vesicle size.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The CSF-1 receptor utilizes ubiquitin as an endocytic signal (Lee et al., 1999), but the NPF triplets in Dab2 could recruit eps15, which, like epsin, can bind ubiquitin directly (Polo et al., 2002).”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Intriguingly, Smad2 and Smad3 activation by liganded TGF-b receptors occurs only post-endocytic internalization (Penheiter et al., 2002), raising the possibility that Dab2, acting at the coated vesicle, coordinates aspects of TGF-b signaling.”
What the sources say
- Not checked — no full text of the sourcecites Penheiter et al., 2002 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
The paper relies on this without support.
The in vitro assembly of clathrin cages by Dab2 on liposome templates reflects the mechanism of clathrin-coated pit assembly at the plasma membrane.
“With synthetic liposome templates, Dab2 drives clathrin-coat assembly in the presence of puri®ed AP-2 and clathrin and, consequently, displays all the properties of a cargo-speci®c adaptor protein.”
The paper relies on this without support.
The LDL receptor cytosolic domain peptide used in binding assays represents the intact LDL receptor's FXNPXY internalization motif.
“Addition of a 3-to 5-fold molar excess of a peptide corresponding to residues 2±22 of the LDL receptor cytosolic domain ( 814 NWRLKNINSIFDNPVYQKTT) does not diminish the extent of monomeric PTB domain association with the liposomes (Figure 6D, lane d compared with b).”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“some PTB domains, including the domain in ARH, bind phosphoinositides (8,11,12).”
From The Modular Adaptor Protein ARH Is Required for Low Density Lipoprotein (LDL) Binding and Internalization but Not for LDL Receptor Clustering in Coated Pits (2004) · cites this paper as [12]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Through its PTB domain, Dab2 mediates the attachment of cargos containing transmembrane proteins with an NPXY motif, such as the LDL receptor, EGF receptor, megalin, and integrins, to clathrin coats”
From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Mishra et al., 2002
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In accordance with this mechanism, coated pits contain many potential binding partners for LDLR including AP2 (34), PTB domain-containing adaptor proteins such as Dab2 (12,28) and the clathrin heavy chain (35).”
From The Modular Adaptor Protein ARH Is Required for Low Density Lipoprotein (LDL) Binding and Internalization but Not for LDL Receptor Clustering in Coated Pits (2004) · cites this paper as [12]
The cited source says what the claim attributes to it.
In the citing paper
“Another endocytic clathrin adaptor, Disabled-2 (Dab2), is potentially an LDLR-selective adaptor”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [22]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Immuno¯uorescence analysis
“(D) The PTB domain of Dab2 binds to phosphoinositides and FXNPXF internalization motifs synchronously.”
§ Dab2 binds to phosphoinositides via the N-terminal PTB domain
“Dab2 PTB association with phosphoinositide-containing mixed liposomes does not preclude NPXY sequence engagement.Addition of a 3-to 5-fold molar excess of a peptide corresponding to residues 2±22 of the LDL receptor cytosolic domain ( 814 NWRLKNINSIFDNPVYQKTT)”
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Metadata
- Authors
- Mishra, S. K., Keyel, P. A., Hawryluk, M. J., Agostinelli, N. R., Watkins, S. C., & Traub, L. M.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Traub, Linton M.
- Venue
- The EMBO Journal
- Published
- 2002-09-16
- Volume
- 21
- Issue
- 18
- Pages
- 4915-4926
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC126284
- OpenAlex
- W1983921682
- Semantic Scholar
- f2627d366f380de384fe68eee4a251f9a7898e0d
- Cited by
- 302
- References
- 68
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 2 · 2023: 1 · 2022: 8 · 2021: 10 · 2020: 6 · 2019: 5 · 2018: 4 · 2017: 5 · 2016: 8 · 2015: 15 · 2014: 10 · 2013: 16 · 2012: 12
- FWCI
- 7.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK053249)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Biotin and Related Studies
- Keywords
- Disabled-2, clathrin adaptor proteins, clathrin-coated pits, cargo selection, phosphoinositides, phosphotyrosine binding domain, AP-2, membrane internalization, clathrin-coated vesicles
- MeSH terms
- Amino Acid Sequence, Animals, Biological Transport, Carrier Proteins, Clathrin, Endocytosis, Fluorescent Dyes, HeLa Cells, Humans, Molecular Sequence Data, Neuropeptides, Peptides, Phosphatidylinositols, Protein Binding, Proteins, Receptors, LDL, Recombinant Fusion Proteins, Genes, Tumor Suppressor, Genes, Reporter, COS Cells, Amino Acid Motifs, Tumor Suppressor Proteins, Vesicular Transport Proteins, Adaptor Proteins, Vesicular Transport, Adaptor Protein Complex 2, Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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