RhoH GTPase: A Key Regulator of Hematopoietic Cell Proliferation and Apoptosis?
Open accessAbstract
Rho GTPases are well characterized as critical regulators of cell growth and actin cytoskeleton in eukaryotic cells. The RhoE/Rnd3 subfamily member RhoH is hematopoietic-specific and GTPase deficient and thus is expected to be in the constitutively active, GTP-bound conformation. The activity of RhoH is likely regulated by the level of expression rather than GTP-binding/GTP-hydrolysis cycle in the cell. By RNAi based knockdown and overexpression approaches we recently have shown in hematopoietic progenitor cells that RhoH negatively impacts on growth factor-induced proliferation and survival and modulates chemokine-induced actin reorganization and cell migration. In addition, RhoH appears to counteract Rac GTPase activities, suggesting a possible mechanism by which RhoH functions as an antagonist of Rac signaling in the regulation of cell growth and actin-based functions in blood lineages.
AI snapshot
Written from the paper’s full text.
TL;DR
RhoH is a hematopoietic-specific, GTPase-deficient Rho family member whose activity is likely controlled by expression level rather than the classic GTP-binding/hydrolysis cycle. This review/commentary summarizes evidence that RhoH negatively regulates hematopoietic progenitor cell proliferation, survival, migration, and actin-based functions, possibly by antagonizing Rac GTPase signaling.
Key findings
- RhoH is hematopoietic-specific and naturally GTPase deficient, so it is expected to remain constitutively GTP-bound; its cellular activity is proposed to be regulated by protein expression level rather than GEF/GAP/GDI-controlled cycling.
- In murine hematopoietic progenitor cells, RhoH overexpression suppressed growth factor-induced proliferation and survival and inhibited chemokine-induced migration and F-actin polymerization in vitro; increased RhoH reduced HPC reconstitution in bone marrow and peripheral blood of lethally irradiated recipient mice, associated with reduced HPC proliferation and increased HPC apoptosis in vivo.
- Decreased RhoH expression was associated with increased HPC proliferation, survival, and migration activities, implying RhoH acts as a negative regulator of these processes.
- RhoH appears to antagonize Rac signaling: it reduced GTP-bound Rac1 and Rac2 in HPCs, and RhoH overexpression and Rac1/2 deficiency in HPCs produced similar phenotypes; RhoH may act both upstream and downstream of Rac GTPases.
- RhoH is hypermutable in human primary lymphoma samples and lymphoma cell lines, with translocations and somatic mutations occurring exclusively in noncoding regulatory sequences, suggesting reduced RhoH expression may have pathophysiological relevance to hematologic malignancies.
Methods
- This is a review/commentary that synthesizes the authors’ recent work and cited literature; it reports no new primary experimental data.
- It discusses RNAi-based knockdown and overexpression approaches in murine hematopoietic progenitor cells, retrovirus-mediated overexpression and RNA interference, studies in Jurkat T cells, human primary lymphoma samples and lymphoma cell lines, and unpublished data in NIH 3T3 cells.
- Main analysis is narrative synthesis; no statistical methods, sample sizes, or quantitative results are described.
Limitations
- The paper states that pathophysiological relevance of dysregulated RhoH expression to hematologic malignancies is “not yet demonstrated experimentally,” and that future studies are needed to define where RhoH intersects with Rac GTPases and whether it engages shared or unique effectors in physiologically relevant systems.
- Several key mechanistic claims rely on “unpublished data,” including RhoH antagonism of Rac1-mediated transcription/proliferation in NIH 3T3 cells and possible interaction with Pak1.
- Evident from the text: as a review/commentary, it provides no new experimental details, sample sizes, or statistical analyses, and some conclusions depend on cited prior work or unpublished observations.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
0 of 33 cited sources checked · 0 supported · 0 flagged
- Findingown data§ Abstract
Increased RhoH expression led to reduced activity of HPC reconstitution in the bone marrow and peripheral blood of lethally irradiated recipient mice.
“Increased RhoH expression led to a reduced activity of HPC reconstitution in the bone marrow and the peripheral blood of the lethally irradiated recipient mice, and this was associated with reduced HPC proliferation and increased HPC apoptosis in vivo.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Findingown data§ Abstract
RhoH modulates chemokine-induced actin reorganization and cell migration in hematopoietic progenitor cells.
“By RNAi based knock-down and overexpression approaches we recently have shown in hematopoietic progenitor cells that RhoH negatively impacts on growth factor-induced proliferation and survival and modulates chemokine-induced actin reorganization and cell migration.”
- Also stated in: § Abstract · plain
“Overexpression of RhoH in HPCs suppressed growth factor-induced proliferation and survival and inhibited chemokine-induced migration and F-actin polymerization in vitro.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Abstract · plain
- Findingown data§ Abstract
Decreased RhoH expression was associated with increased HPC proliferation, survival and migration activities.
“On the other hand, decreased RhoH expression was associated with increased HPC proliferation, survival and migration activities.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Findingown data§ Abstract
RhoH negatively impacts growth factor-induced proliferation and survival in hematopoietic progenitor cells.
“By RNAi based knock-down and overexpression approaches we recently have shown in hematopoietic progenitor cells that RhoH negatively impacts on growth factor-induced proliferation and survival and modulates chemokine-induced actin reorganization and cell migration.”
- Also stated in: § Abstract · plain
“Overexpression of RhoH in HPCs suppressed growth factor-induced proliferation and survival and inhibited chemokine-induced migration and F-actin polymerization in vitro.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Abstract · plain
- Findingown data§ Abstract
In NIH 3T3 cells, RhoH expression antagonizes Rac1-mediated gene transcription and proliferation.
“Indeed, in NIH 3T3 cells RhoH expression is found to antagonize Rac1-mediated gene transcription and proliferation (unpublished data).”
Quote in the paperNot a substantial claim
- Findingcitation§ Abstract
In HPCs, RhoH reduces the level of GTP-bound Rac1 and Rac2.
“In HPCs we have observed that RhoH is able to reduce the level of the GTP-bound Rac1 and Rac2, 9 suggesting an antagonistic effect of RhoH upstream of Rac GTPases.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation§ Abstract
RhoH is naturally GTPase deficient.
“However, RhoH, an hematopoietic-specific and relatively anonymous member of the Rho family, is naturally GTPase deficient.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [4]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation§ Abstract
RhoH is differentially expressed in hematopoietic cells.
“While RhoH is hematopoietic cell-specific, it is differentially expressed.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning§ Abstract
RhoH functions as an antagonist of Rac signaling in the regulation of cell growth and actin-based functions in blood lineages.
“In addition, RhoH appears to counteract Rac GTPase activities, suggesting a possible mechanism by which RhoH functions as an antagonist of Rac signaling in the regulation of cell growth and actin-based functions in blood lineages.”
Quote in the paperSubstantial claim - Interpretationreasoning§ Abstract
RhoH is expected to be in the constitutively active, GTP-bound conformation.
“Thus RhoH stays constitutively in the active, GTP-bound state without the GTP-hydrolytic regulation.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [4]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation§ Abstract
RhoH is hematopoietic-specific.
“However, RhoH, an hematopoietic-specific and relatively anonymous member of the Rho family, is naturally GTPase deficient.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [4]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation§ Abstract
RhoH mutations in lymphoma occur exclusively in the noncoding regulatory sequences.
“These mutations occur exclusively in the noncoding regulatory sequences.”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [7]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning§ Abstract
The cellular activity of RhoH is likely regulated by its level of protein expression rather than by the GEF/GAP/GDI-controlled GTP-binding/GTP-hydrolysis cycle.
“The activity of RhoH is likely regulated by the level of expression rather than GTP-binding/GTP-hydrolysis cycle in the cell.”
- Also stated in: § Abstract · hedged
“It has been proposed that the cellular activity of RhoH is likely regulated by the level of the protein expression in cells rather than by the GEF/GAP/GDI controlled, classic GTP-binding/GTP-hydrolysis cycle.”
Quote in the paperSubstantial claim - Also stated in: § Abstract · hedged
- Premisecitation§ Abstract
The RhoH gene is hypermutable, harboring chromosome translocations and somatic mutations at a higher than expected frequency in human primary lymphoma samples and lymphoma cell lines.
“Interestingly, studies utilizing human primary lymphoma samples and lymphoma cell lines have shown that the RhoH gene is hypermutable, harboring chromosome translocations and somatic mutations at a higher than expected frequency.”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [7]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [8]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation§ Abstract
Lymphoid lineages show higher levels of RhoH expression than primitive progenitor cells and myeloid lineages.
“Lymphoid lineages show higher levels of RhoH expression, while primitive progenitor cells and myeloid lineages show lower expression.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning§ Abstract
RhoH expression may be important for its function.
“Although not yet demonstrated experimentally, these findings also suggest that RhoH expression may be important for its function, and that dysregulated RhoH expression, specifically reduced expression, may have pathophysiological relevance to hematologic malignancies.”
Quote in the paperSubstantial claim - Interpretationown data§ Abstract
RhoH counteracts Rac GTPase activities.
“In addition, RhoH appears to counteract Rac GTPase activities, suggesting a possible mechanism by which RhoH functions as an antagonist of Rac signaling in the regulation of cell growth and actin-based functions in blood lineages.”
- Also stated in: § Abstract · hedged
“In HPCs we have observed that RhoH is able to reduce the level of the GTP-bound Rac1 and Rac2, 9 suggesting an antagonistic effect of RhoH upstream of Rac GTPases.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Abstract · hedged
- Interpretationreasoning§ Abstract
RhoH acts as a negative regulator of cell proliferation and survival in blood cells.
“The opposite effects of RhoH overexpression and knockdown in HPCs imply that RhoH acts as a negative regulator of cell proliferation and survival as well as a modulator of actin cytoskeletion and migration in blood cells.”
Quote in the paperSubstantial claim - Premisecitation§ Abstract
RhoE/Rnd1-3 represent a distinct group of Rho proteins displaying functional effects antagonistic to those of other Rho GTPases.
“In contrast, RhoE/Rnd1-3 represent a distinct group of Rho proteins displaying functional effects antagonistic to those of other Rho GTPases.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [13]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [14]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationown data§ Abstract
RhoH has an antagonistic effect upstream of Rac GTPases.
“In HPCs we have observed that RhoH is able to reduce the level of the GTP-bound Rac1 and Rac2, 9 suggesting an antagonistic effect of RhoH upstream of Rac GTPases.”
Quote in the paperSubstantial claim
- May combine two claims. 5
- Classified as probably not a substantial claim. 6
May combine two claims.
Findingown data§ AbstractIncreased RhoH expression was associated with reduced HPC proliferation and increased HPC apoptosis in vivo.
“Increased RhoH expression led to a reduced activity of HPC reconstitution in the bone marrow and the peripheral blood of the lethally irradiated recipient mice, and this was associated with reduced HPC proliferation and increased HPC apoptosis in vivo.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Findingown data§ AbstractRhoH may interact directly with a subset of Rac effectors such as p21-activated kinase 1 (Pak1).
“Furthermore, RhoH may interact directly with a subset of Rac effectors such as p21-activated kinase 1 (Pak1) (unpublished data).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Premisenone given§ AbstractRhoH belongs to the RhoE/Rnd3 subfamily.
“RhoH belongs to the RhoE/Rnd3 subfamily, all of which share the characteristic.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Interpretationreasoning§ AbstractDysregulated RhoH expression, specifically reduced expression, may have pathophysiological relevance to hematologic malignancies.
“Although not yet demonstrated experimentally, these findings also suggest that RhoH expression may be important for its function, and that dysregulated RhoH expression, specifically reduced expression, may have pathophysiological relevance to hematologic malignancies.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim. May combine two claims.
Premisecitation§ AbstractRac1, Rac2, Cdc42 and RhoA are positive regulators of cell cycle progression, survival and actin polymerization/bundling.
“The Rho family members Rac1, Rac2, Cdc42 and RhoA have been known to be positive regulators of cell cycle progression, survival and actin polymerization/bundling.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [11]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [12]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Interpretationown data§ AbstractRhoH acts as a modulator of actin cytoskeleton and migration in blood cells.
“The opposite effects of RhoH overexpression and knockdown in HPCs imply that RhoH acts as a negative regulator of cell proliferation and survival as well as a modulator of actin cytoskeletion and migration in blood cells.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
Premisecitation§ AbstractRhoH may inhibit Rac1 signaling at a level downstream of Rac1 that may involve p38 MAPK and NF-κB in Jurkat T cell.
“It has been previously reported that RhoH may inhibit Rac1 signaling at a level downstream of Rac1 that may involve p38 mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) in Jurkat T cell.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [5]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ AbstractRhoE inhibits G1 phase progression and promotes loss of stress fiber assembly and focal adhesion, at least in part by altering activities of upstream and downstream components of RhoA signaling module.
“For example, RhoE inhibits G 1 phase progression and promotes loss of stress fiber assembly and focal adhesion, 14,15 at least in part by altering the activities of both upstream and downstream components of RhoA signaling module.”
Quote in the paperNot a substantial claim0 of 4 sources checked- cites [14]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [15]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [16]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites [17]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Interpretationcitation§ AbstractRhoH appears to have a negative impact on cell proliferation and F-actin polymerization, opposite to that elicited by Rac1 and Rac2 in HPCs.
“Like RhoE, RhoH appears to have a negative impact on cell proliferation and F-actin polymerization, which seems to be opposite of that elicited by Rac1 and Rac2 in HPCs.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [12]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Cites
The publisher hasn’t deposited this paper’s reference list.
Research works printed but not linked: 2
- Zheng Y. Dbl family guanine nucleotide exchange factors. Trends Biochem Sci 2001; 26:724-32.
- Dallery E, Galiegue-Zouitina S, Collyn-d'Hooghe M, Quief S, Denis C, Hildebrand MP, Lantoine D, Deweindt C, Tilly H, Bastard C, Kerckaert JP. TTF, a gene encoding a novel small G protein, fuses to the lymphoma-associated LAZ3 gene by t(3;4) chromosomal translocation. Oncogene 1995; 10:2171-8.
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- Authors
- Gu, Y., Zheng, Y., & Williams, D. A.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2004-11-19
- Volume
- 4
- Issue
- 2
- Pages
- 204-205
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W4253471947
- Cited by
- 20
- References
- 0
- Citations by year
- 2026: 1 · 2024: 3 · 2021: 2 · 2020: 1 · 2014: 3 · 2013: 1 · 2012: 2
- FWCI
- 0.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- RhoH, Rho GTPases, hematopoietic progenitor cells, cell proliferation, apoptosis, cell survival, actin cytoskeleton, cell migration, chemokine signaling, Rac GTPase
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