Overview of RASA4B (RAS p21 Protein Activator 4B) in Human

Gene Family and Structural Features

RASA4B is a protein-coding human gene on chromosome 7 (7q22.1) that encodes a putative Ras GTPase-activating protein (GAP) (www.ncbi.nlm.nih.gov) (www.proteinatlas.org). It belongs to the GAP1 family of Ras GAPs, which includes closely related genes like RASA4 (also known as CAPRI, the calcium-promoted Ras inactivator) (pmc.ncbi.nlm.nih.gov). RASA4B shares a high degree of sequence and domain similarity with RASA4, suggesting it arose from a duplication event in the genome and likely performs a similar biological role. Like other GAP1 family members, the RASA4B protein contains a modular architecture: an N-terminal tandem C2 domain region (two Ca²⁺-dependent phospholipid-binding C2 domains) followed by a pleckstrin homology (PH) domain, and a C-terminal RasGAP catalytic domain (pmc.ncbi.nlm.nih.gov). The C2 domains allow the protein to sense calcium and target membranes, while the PH domain may bind membrane phosphoinositides, collectively positioning the RasGAP domain at the plasma membrane in response to signals (pmc.ncbi.nlm.nih.gov). RASA4B is a ~803 amino acid protein (≈90 kDa) with these domains, and it is predicted to bind phospholipids and metal ions (notably zinc) as part of its structure (www.ncbi.nlm.nih.gov). The presence of a conserved “arginine finger” motif in the RasGAP domain – a critical arginine residue that inserts into the Ras active site – is expected, as this is the catalytic mechanism by which RasGAPs accelerate GTP hydrolysis on Ras (pmc.ncbi.nlm.nih.gov). In summary, RASA4B’s sequence features suggest it is a calcium-regulated Ras GAP with the capacity for membrane recruitment and Ras protein interaction, much like its paralog RASA4/CAPRI.

Molecular Function and Enzymatic Activity

As a Ras-specific GTPase-activating protein, the primary biochemical function of RASA4B is to inactivate Ras proteins by accelerating their GTPase activity. In general, Ras proteins cycle between an active GTP-bound state and an inactive GDP-bound state, and GAPs tilt this balance toward the inactive state (pmc.ncbi.nlm.nih.gov). RASA4B is predicted to enable GTPase activator activity, meaning it binds to active Ras·GTP and promotes the hydrolysis of Ras-bound GTP to GDP (www.ncbi.nlm.nih.gov). This greatly speeds up Ras’s intrinsic GTPase rate – an effect achieved by stabilizing the transition state of the reaction. Like other RasGAPs, RASA4B’s catalytic domain likely inserts an “arginine finger” residue into Ras’s active site, contributing positive charge that helps hydrolyze the GTP (pmc.ncbi.nlm.nih.gov). This mechanism of action is well-established for Ras GAPs: they act as negative regulators of Ras signaling by accelerating GTP hydrolysis, thereby turning off Ras activity (pmc.ncbi.nlm.nih.gov). In essence, RASA4B functions as an enzyme that converts active Ras-GTP into inactive Ras-GDP, terminating the signal that Ras would otherwise transmit.

Notably, studies of the GAP1 family have shown that these proteins can have dual substrate specificity for certain Ras-related GTPases. In particular, the RASA4 (CAPRI) protein can act on both Ras and Rap1 GTPases, depending on context (pmc.ncbi.nlm.nih.gov) (pubmed.ncbi.nlm.nih.gov). CAPRI was shown to function as a Ca²⁺-regulated GAP for Rap1 as well as Ras – it remains largely inactive toward Rap1 in the cytosol, but upon calcium-triggered membrane translocation it can also promote Rap1 GTP hydrolysis (pubmed.ncbi.nlm.nih.gov). This bifunctional Ras/Rap GAP activity was demonstrated for CAPRI and another family member (RASAL1) in biochemical assays (pmc.ncbi.nlm.nih.gov) (pubmed.ncbi.nlm.nih.gov). By analogy, RASA4B’s GAP domain is expected to target the classic Ras proteins (H-Ras, K-Ras, N-Ras) as its primary substrates, and it may have the capacity to inactivate Rap1 as well, although RASA4B-specific experiments have not yet confirmed this. The requirement of regions outside the core GAP domain (such as the C2 domains or PH domain) for RapGAP activity in related proteins (pubmed.ncbi.nlm.nih.gov) (pubmed.ncbi.nlm.nih.gov) suggests that RASA4B’s full-length structure is important for any broader substrate specificity. In summary, RASA4B’s enzymatic role is to switch off Ras (and potentially Rap1) signaling by catalyzing GTP hydrolysis – a reaction that is fundamentally important for controlling downstream signaling pathways.

Biological Function in Signaling Pathways

Through its Ras-inactivating activity, RASA4B is predicted to play a negative regulatory role in the Ras–Mitogen-Activated Protein Kinase (MAPK) signaling pathway. Ras proteins are key molecular switches that trigger the MAPK cascade, driving cellular proliferation, differentiation, and gene expression programs (pmc.ncbi.nlm.nih.gov) (www.proteinatlas.org). By turning off Ras, RASA4B effectively serves as a brake on these signaling outputs. In fact, elevations in intracellular calcium are thought to be a trigger for RASA4B to exert its function in cells (www.proteinatlas.org). RASA4B is calcium-dependent – it contains C2 domains that bind Ca²⁺ – and this links calcium signaling to Ras pathway modulation. The current understanding (largely based on its paralog CAPRI/RASA4) is that when a stimulus causes a rise in cytosolic Ca²⁺, RASA4B will translocate from the cytosol to the inner surface of the plasma membrane (where Ras is located) and there activate its GAP activity (www.proteinatlas.org) (pmc.ncbi.nlm.nih.gov). During the period it is membrane-bound, RASA4B can bind active Ras and accelerate GTP hydrolysis, thereby switching Ras from the active GTP-bound form to the inactive GDP-bound form (www.proteinatlas.org). Consequently, Ras can no longer trigger downstream effector pathways such as the Raf/MEK/ERK (MAPK) cascade (www.proteinatlas.org). This mechanism provides a feedback or signal integration role: RASA4B (like CAPRI) “decodes” calcium signals to modulate Ras activity, ensuring that calcium spikes or sustained calcium levels lead to timely termination of Ras-MAPK signaling (www.proteinatlas.org). This is particularly important because many receptor stimuli (e.g. growth factors, immune receptors) induce calcium oscillations or transients as well as Ras activation; calcium-responsive GAPs like RASA4B help coordinate these signals (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov).

In addition to its core role in the Ras/MAPK pathway, RASA4B may have broader functions in cell signaling by acting as a scaffold or adapter protein. Intriguingly, the closely related RASA4 (CAPRI) has been shown to interact with other small GTPases outside the Ras family. For example, CAPRI functions as an adaptor for the Rho-family GTPases Cdc42 and Rac1 during Fcγ receptor (FcR)-mediated phagocytosis in macrophages (www.proteinatlas.org) (pmc.ncbi.nlm.nih.gov). In that setting, CAPRI is recruited to phagocytic cups (sites of active actin remodeling) in a Ca²⁺-dependent manner and constitutively associates with Cdc42/Rac1, helping to coordinate their activation for efficient phagocytosis (pmc.ncbi.nlm.nih.gov). CAPRI-deficient mice showed impaired FcγR phagocytosis and innate immune responses (pmc.ncbi.nlm.nih.gov). While RASA4B’s involvement in this specific process has not been experimentally verified, its high homology to CAPRI suggests it could perform a similar molecular adaptor role, linking Ras signaling with cytoskeletal dynamics or other pathways. In general, by virtue of its multi-domain structure, RASA4B might serve as a node of crosstalk between calcium signaling, Ras/Rap GTPase signaling, and possibly actin-regulating pathways. Its negative regulation of Ras is likely its most direct function, but the protein could have pleiotropic effects on cell behavior whenever Ras activity or Rap1 activity and calcium signals intersect. For instance, by shutting off Ras in response to calcium, RASA4B might influence processes like lymphocyte activation, neuronal signaling, or muscle cell differentiation – any contexts where calcium rises and Ras pathways need tight control. These inferences await direct study, but they align with the known functions of RasGAPs in controlling cell proliferation and differentiation signals (www.proteinatlas.org).

Subcellular Localization and Regulation

Under resting conditions (basal calcium), RASA4B is predominantly localized in the cytosol (www.ncbi.nlm.nih.gov). It is predicted to be an intracellular protein with no signal peptide or transmembrane segments, consistent with a cytosolic localization (www.proteinatlas.org). Upon increases in intracellular Ca²⁺, however, RASA4B is expected to translocate to the plasma membrane by means of its C2 domains binding to calcium and acidic phospholipids on the inner leaflet of the membrane (pmc.ncbi.nlm.nih.gov) (www.proteinatlas.org). This calcium-triggered membrane recruitment is a critical regulatory step: RASA4B essentially lies in wait in the cytoplasm and only when Ca²⁺ signals indicate the appropriate cue does it move to the membrane to find its substrate (Ras). Experimental evidence from CAPRI (RASA4) supports this model: CAPRI rapidly moves from cytosol to plasma membrane after cell stimulation that raises [Ca²⁺]i, and this translocation is absolutely required for it to exert RasGAP activity (pmc.ncbi.nlm.nih.gov). The C2 domains in RASA4B bind membrane phospholipids in a Ca²⁺-dependent manner, functioning like a calcium-sensing lipid anchor (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Once at the membrane, RASA4B can interact with membrane-bound Ras-GTP and turn it off. When Ca²⁺ levels drop, proteins like CAPRI dissociate from the membrane and return to an inactive cytosolic state (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). RASA4B likely follows the same cycle. This spatial regulation ensures that RASA4B’s GAP activity is tightly controlled – it acts only in the right place (membrane microdomains where Ras resides) and time (when Ca²⁺ signals occur). In terms of steady-state distribution, RASA4B is cytosolic but capable of reversible plasma membrane association, aligning with Gene Ontology annotations that place it in the cytosol and plasma membrane compartments (www.ncbi.nlm.nih.gov) (www.proteinatlas.org). No other specific organelle localization has been reported for RASA4B; it does not contain nuclear localization signals or organelle-targeting peptides, so it is thought to function at the inner cell membrane and cytoplasm where Ras signaling takes place.

Expression Patterns and Physiological Context

Expression profiling indicates that RASA4B is expressed in a broad range of human tissues, with certain tissue biases. Data from the NCBI and Human Protein Atlas show RASA4B mRNA is ubiquitous but varies in level (www.ncbi.nlm.nih.gov) (www.proteinatlas.org). Notably, RASA4B is classified as “tissue enriched” in skeletal muscle by transcriptomic analysis, meaning its expression in muscle is higher than in most other tissues (www.proteinatlas.org). In fact, consensus RNA data (GTEx, HPA, FANTOM5) highlight skeletal muscle as a top expression site for RASA4B, while still detecting the gene in many other tissues at lower levels (www.proteinatlas.org). NCBI’s expression panel likewise shows RASA4B transcripts in numerous tissues – for example, relatively high RNA levels in uterus (endometrium), brain, and at least two dozen other tissue types were reported (www.ncbi.nlm.nih.gov). This widespread expression suggests RASA4B has a general cellular role (consistent with Ras signaling being fundamental to many cell types), but the muscle enrichment hints at a potential specialized role in muscle physiology. Muscle cells experience large calcium fluxes during contraction, so one hypothesis is that RASA4B helps modulate Ras/MAPK signaling in muscle in response to excitation or exercise (where calcium spikes are frequent). Similarly, RASA4B’s expression in the brain and immune-related organs could mean it contributes to calcium-coupled Ras signaling in neurons or immune cells. Such roles would be analogous to known functions of CAPRI/RASA4 in T-cells and macrophages, where it integrates calcium signals to restrain Ras activation (www.proteinatlas.org) (pmc.ncbi.nlm.nih.gov).

It is worth noting that no specific developmental or cell-type exclusive expression of RASA4B has been documented in the literature yet, beyond the broad patterns above. Both RASA4B and its paralog RASA4 are expressed in many overlapping tissues, which may indicate some redundancy or cooperation. In mice, both genes are present, and knockout studies for the Capr1 gene (Rasa4) cause immune functional defects (pmc.ncbi.nlm.nih.gov); a separate knockout for the Rasa4b gene has been generated in large-scale projects, which showed phenotypes related to immune and hematopoietic systems (www.genecards.org), though detailed analyses have not been published. These observations imply RASA4B could play a role in blood or immune cell function as well, potentially overlapping with RASA4. Overall, the physiological context for RASA4B is likely any scenario where intracellular calcium elevations need to be translated into a down-regulation of Ras or Rap signaling. This could include immune cell activation (where calcium rises during antigen receptor signaling), neuronal activity, fertilization (calcium waves in egg cells), muscle excitation, and growth factor or hormone stimulation in various tissues.

Emerging Research and Clinical Relevance

As of the latest research updates (2023–2024), RASA4B remains relatively under-characterized in comparison to other Ras regulators, but several lines of evidence point to its importance. Large-scale cancer genomics projects have examined RASA4B expression and found it to be present across essentially all analyzed tumor types (consistent with it being a housekeeping signaling regulator) (www.proteinatlas.org). Interestingly, RASA4B has surfaced as a potential prognostic biomarker in certain cancers. Data from the Human Protein Atlas (based on TCGA patient outcomes) indicate that high RASA4B expression correlates with improved survival in pancreatic cancer, whereas in stomach (gastric) cancer high RASA4B correlates with worse survival (www.proteinatlas.org). In pancreatic adenocarcinoma, RASA4B was identified as a favorable prognostic marker (p < 0.001), while in stomach cancer it was an unfavorable marker (p < 0.001) (www.proteinatlas.org). These associations suggest that RASA4B’s activity (or loss thereof) might influence tumor behavior – for example, strong RasGAP activity could suppress oncogenic Ras signals in some contexts (beneficial in Ras-driven cancers like pancreatic cancer), but in other contexts tumor cells with high RASA4B might attenuate Ras to a degree that favors alternate growth pathways (potentially explaining the adverse correlation in gastric cancer). It should be emphasized that these are correlative findings and no direct causal link has been proven yet between RASA4B and cancer progression. However, they underscore a real-world interest in RASA4B as part of the Ras regulatory network that is frequently dysregulated in diseases.

Beyond oncology, RASA4B and its family members are being studied for their roles in disorders of the Ras pathway (collectively known as “Rasopathies”) and immune system function. Given that multiple RasGAPs function as tumor suppressors (e.g. NF1 in neurofibromatosis, RASA1 in vascular syndromes) (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov), RASA4B could similarly act as a tumor suppressor by restraining excessive Ras/MAPK signaling. No germline mutations in RASA4B have been definitively linked to human disease as of now, but this gene’s close relative RASAL2 has been implicated in developmental disorders and cancers, showing that Ras/MAPK inhibitors often have critical roles in vivo (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). On the laboratory research front, tools such as CRISPR knockouts and antibody probes for RASA4B are available and have been used to begin exploring its function (www.genecards.org). The experimental evidence at the protein level for RASA4B has been reported (e.g. mass spectrometry peptide detection) (www.proteinatlas.org) (www.proteinatlas.org), confirming that the gene is indeed translated into protein in human cells. Future studies are expected to clarify how RASA4B is regulated (for instance, whether it is activated by specific calcium-mobilizing receptors or by other post-translational modifications) and what unique roles it may play that distinguish it from the canonical CAPRI/RASA4.

In summary, RASA4B is a calcium-regulated Ras GTPase-activating protein that serves as a terminator of Ras signaling and possibly an integrator of Ras with other signaling pathways. It localizes to the cytosol and translocates to the plasma membrane upon calcium influx to turn off Ras by stimulating GTP hydrolysis (www.proteinatlas.org). Through this action, RASA4B likely helps cells fine-tune proliferative and differentiation signals in response to second messengers like Ca²⁺. Its broad expression and involvement in fundamental signaling circuits highlight its biological significance, even as ongoing research works to fully delineate its functions. Authoritative reviews of Ras regulators describe proteins like RASA4B as crucial modulators that connect intracellular calcium dynamics to the Ras/MAPK pathway, ensuring that transient signals are properly decoded at the level of Ras activation (www.proteinatlas.org) (pmc.ncbi.nlm.nih.gov). While direct studies of RASA4B are still emerging, the current understanding – grounded in its domain structure, homology to CAPRI, and database annotations – paints RASA4B as an important intracellular signaling hub that safeguards cells from aberrant Ras activity and coordinates signaling crosstalk in calcium-rich environments. This makes RASA4B an interesting target for further investigation, with potential implications in areas ranging from cancer biology to immunology and muscle physiology.

Sources:

• Alliance of Genome Resources (2025) – Gene summary for RASA4B: RASA4B is predicted to have GTPase activator activity, phospholipid binding, and zinc ion binding functions, and to be involved in calcium-responsive signal transduction and negative regulation of Ras signaling (www.ncbi.nlm.nih.gov) (www.ncbi.nlm.nih.gov). It is a protein-coding gene located on 7q22.1 and encodes a 803-aa protein predicted in cytosol and plasma membrane compartments (www.ncbi.nlm.nih.gov) (www.genecards.org).
• Scheffzek & Shivalingaiah (Cold Spring Harb Perspect Med, 2019) – Review on Ras-specific GAPs: RasGAPs act as negative regulators of Ras by accelerating GTP hydrolysis on Ras, thereby down-regulating Ras activity (pmc.ncbi.nlm.nih.gov). They share a conserved RasGAP domain (with a critical “arginine finger” for catalysis) and often include regulatory domains (C2, PH, etc.) for subcellular targeting (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). The GAP1 subfamily (including RASA4/CAPRI) contains two C2 domains and a PH domain preceding the RasGAP module (pmc.ncbi.nlm.nih.gov). CAPRI/RASA4 and related GAP1 members can inactivate both Ras and Rap GTPases (dual specificity), and CAPRI’s activity is Ca²⁺-dependent, requiring Ca²⁺-triggered membrane translocation to exert its Ras/Rap-GAP function (pmc.ncbi.nlm.nih.gov).
• Human Protein Atlas (2022) – Protein profile of RASA4B: RASA4B is categorized as an intracellular RAS pathway-related protein, with evidence at the protein level. It has 3 known transcript variants and is highly expressed in skeletal muscle (tissue-enriched in muscle) while being detected in many tissues overall (www.proteinatlas.org). Due to antibody cross-reactivity with RASA4, immunohistochemistry results are uncertain (www.proteinatlas.org). In cancer datasets, RASA4B expression has low cancer-type specificity (present in all surveyed tumors) and has prognostic value in pancreatic cancer (favorable outcome) and stomach cancer (unfavorable outcome) with high statistical significance (www.proteinatlas.org).
• NCBI RefSeq (Gene ID 100271927) – Entrez gene summary for RASA4B (as of Jul 2008): RASA4B encodes a member of the GAP1 family that suppresses the Ras/MAPK pathway in response to Ca²⁺ signals (www.proteinatlas.org). When intracellular Ca²⁺ increases, the protein translocates to the plasma membrane and activates Ras GTPase activity, converting Ras from the active GTP-bound state to inactive GDP-bound state (www.proteinatlas.org). This prevents Ras from activating downstream pathways that control gene expression, cell growth, and differentiation (www.proteinatlas.org). (Multiple transcript variants exist for this gene.)
• Cullen PJ et al. (EMBO J, 2004) – Identification of a Ca²⁺-regulated Ras GAP (CAPRI): This study characterized CAPRI (human RASA4) as a Ca²⁺-triggered Ras inactivator. CAPRI is cytosolic at rest and rapidly translocates to the plasma membrane in synchrony with calcium oscillations (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Only during its membrane association does CAPRI inactivate Ras. CAPRI did not respond to single transients but acted as a decoder of high-frequency Ca²⁺ oscillations, linking repetitive Ca²⁺ spikes to intermittent Ras inactivation (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). This revealed a novel mechanism by which complex Ca²⁺ signals regulate Ras activity in cells.
• Zhang J. et al. (Nat Immunol, 2005) – CAPRI in immune cell phagocytosis: Demonstrated that CAPRI (RASA4) serves as an adaptor linking Fcγ receptors to Rho GTPases Cdc42/Rac1 during phagocytosis (pmc.ncbi.nlm.nih.gov). CAPRI knockout macrophages had defective FcγR-mediated phagocytosis and ROS production. CAPRI was found to constitutively bind Cdc42/Rac1 and translocate to phagocytic cups, facilitating the activation of these GTPases for actin remodeling (pmc.ncbi.nlm.nih.gov). CAPRI-deficient mice showed impaired bacterial clearance, highlighting CAPRI’s essential role in the innate immune response (pmc.ncbi.nlm.nih.gov). These findings extend the function of RASA4 beyond Ras-MAPK suppression to coordinating cross-talk between calcium, Ras, and actin cytoskeleton dynamics in immune cells. (By extension, RASA4B may share some of these adaptor functions given its similarity, though direct evidence is pending.)

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28. AnnotationURLCitation(end_index=9549, start_index=9377, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=In%20unstimulated%20cells%2C%20CAPRI%20is,this%20membrane%20association%20activates%20the')
29. AnnotationURLCitation(end_index=10166, start_index=9983, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=PROTEIN%20FUNCTION%20Protein%20function%20%28UniProt%29,of%20the%20GAP1%20family%20of')
30. AnnotationURLCitation(end_index=10282, start_index=10167, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=Fc%20receptor%20%28FcR%29,These')
31. AnnotationURLCitation(end_index=10629, start_index=10514, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=Fc%20receptor%20%28FcR%29,These')
32. AnnotationURLCitation(end_index=10829, start_index=10714, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=Fc%20receptor%20%28FcR%29,These')
33. AnnotationURLCitation(end_index=11975, start_index=11869, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
34. AnnotationURLCitation(end_index=12276, start_index=12118, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=activity%3B%20and%20zinc%20ion%20binding,of%20Genome%20Resources%2C%20Jul%202025')
35. AnnotationURLCitation(end_index=12548, start_index=12416, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=Gene%20description,Detected%20in%20many')
36. AnnotationURLCitation(end_index=12938, start_index=12766, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=In%20unstimulated%20cells%2C%20CAPRI%20is,this%20membrane%20association%20activates%20the')
37. AnnotationURLCitation(end_index=13045, start_index=12939, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
38. AnnotationURLCitation(end_index=13697, start_index=13525, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=In%20unstimulated%20cells%2C%20CAPRI%20is,this%20membrane%20association%20activates%20the')
39. AnnotationURLCitation(end_index=14000, start_index=13828, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=In%20unstimulated%20cells%2C%20CAPRI%20is,this%20membrane%20association%20activates%20the')
40. AnnotationURLCitation(end_index=14163, start_index=14001, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=CAPRI%2C%20the%20corresponding%20domains%20of,and%20that%20this%20activity%20is')
41. AnnotationURLCitation(end_index=14529, start_index=14366, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=match%20at%20L140%20to%20function,oscillates%20between%20the%20plasma%20membrane')
42. AnnotationURLCitation(end_index=14691, start_index=14530, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=to%20function%20as%20a%20RasGAP,oscillates%20between%20the%20plasma%20membrane')
43. AnnotationURLCitation(end_index=15310, start_index=15152, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=activity%3B%20and%20zinc%20ion%20binding,of%20Genome%20Resources%2C%20Jul%202025')
44. AnnotationURLCitation(end_index=15460, start_index=15311, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GO%3A0005543%20,regulation%20of%20GTPase%20activity')
45. AnnotationURLCitation(end_index=16148, start_index=15991, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=Expression%20Ubiquitous%20expression%20in%20endometrium,Try%20the%20new%20%2014')
46. AnnotationURLCitation(end_index=16300, start_index=16149, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=RNA%20category,at%20protein%20level%20Protein%20expression')
47. AnnotationURLCitation(end_index=16625, start_index=16474, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=RNA%20category,at%20protein%20level%20Protein%20expression')
48. AnnotationURLCitation(end_index=16959, start_index=16808, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=RNA%20category,at%20protein%20level%20Protein%20expression')
49. AnnotationURLCitation(end_index=17326, start_index=17169, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=Expression%20Ubiquitous%20expression%20in%20endometrium,Try%20the%20new%20%2014')
50. AnnotationURLCitation(end_index=18190, start_index=18084, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
51. AnnotationURLCitation(end_index=18341, start_index=18191, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=phagocytosis.%20CAPRI,essential%20for%20innate%20immune%20response')
52. AnnotationURLCitation(end_index=18917, start_index=18760, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=protein%2C%20functions%20as%20an%20adaptor,and%20Cdc42%20and%20Rac1%20and')
53. AnnotationURLCitation(end_index=19195, start_index=19071, title='RASA4B Gene - GeneCards | RAS4B Protein | RAS4B Antibody', type='url_citation', url='https://www.genecards.org/cgi-bin/carddisp.pl?gene=RASA4B#:~:text=,hematopoietic%20system%20phenotype')
54. AnnotationURLCitation(end_index=20385, start_index=20239, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=Cell%20line%20,i%7D%20Evidence%20at%20protein%20level')
55. AnnotationURLCitation(end_index=20854, start_index=20721, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=PROGNOSTIC%20SUMMARY,favorable%20%20%203')
56. AnnotationURLCitation(end_index=21152, start_index=21019, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=PROGNOSTIC%20SUMMARY,favorable%20%20%203')
57. AnnotationURLCitation(end_index=22274, start_index=22186, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=1,41')
58. AnnotationURLCitation(end_index=22399, start_index=22275, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=mutations%20in%20the%20RASA1%20gene,2005')
59. AnnotationURLCitation(end_index=22865, start_index=22750, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=preceded%20by%20a%20C2%20and,53')
60. AnnotationURLCitation(end_index=23001, start_index=22866, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=of%20the%20protein,Jeyabalan%20and%20Clement%202016')
61. AnnotationURLCitation(end_index=23289, start_index=23164, title='RASA4B Gene - GeneCards | RAS4B Protein | RAS4B Antibody', type='url_citation', url='https://www.genecards.org/cgi-bin/carddisp.pl?gene=RASA4B#:~:text=MGI%20Knock%20Outs%20for%20RASA4B%3A')
62. AnnotationURLCitation(end_index=23558, start_index=23414, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=TCGA%20,at%20protein%20level%20Protein%20expression')
63. AnnotationURLCitation(end_index=23690, start_index=23559, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=Protein%20evidence,Reliability%20score')
64. AnnotationURLCitation(end_index=24470, start_index=24364, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
65. AnnotationURLCitation(end_index=25145, start_index=25039, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
66. AnnotationURLCitation(end_index=25287, start_index=25146, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=match%20at%20L567%20activity,to%20an%20increase%20in%20its')
67. AnnotationURLCitation(end_index=26224, start_index=26093, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=Summary%20Predicted%20to%20enable%20GTPase,Expression')
68. AnnotationURLCitation(end_index=26383, start_index=26225, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=activity%3B%20and%20zinc%20ion%20binding,of%20Genome%20Resources%2C%20Jul%202025')
69. AnnotationURLCitation(end_index=26676, start_index=26514, title='RASA4B RAS p21 protein activator 4B [Homo sapiens (human)] - Gene - NCBI', type='url_citation', url='https://www.ncbi.nlm.nih.gov/gene/100271927#:~:text=Predicted%20to%20enable%20GTPase%20activator,of%20Genome%20Resources%2C%20Jul%202025')
70. AnnotationURLCitation(end_index=26828, start_index=26677, title='RASA4B Gene - GeneCards | RAS4B Protein | RAS4B Antibody', type='url_citation', url='https://www.genecards.org/cgi-bin/carddisp.pl?gene=RASA4B#:~:text=Size%3A%20803%20amino%20acids%20Molecular,mass%3A%2090406%20Da')
71. AnnotationURLCitation(end_index=27161, start_index=27053, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=GTPase,Currently%20there')
72. AnnotationURLCitation(end_index=27490, start_index=27328, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=RasGAPs%20typically%20display%20a%20modular,bind%20to%20Rho%20family%20members')
73. AnnotationURLCitation(end_index=27653, start_index=27491, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=interact%20with%20conserved%20regions%20in,the%20impact%20of%20the%20catalytic')
74. AnnotationURLCitation(end_index=27854, start_index=27766, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=3,20')
75. AnnotationURLCitation(end_index=28167, start_index=28079, title='Ras-Specific GTPase-Activating Proteins—Structures, Mechanisms, and Interactions - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC6396337/#:~:text=3,20')
76. AnnotationURLCitation(end_index=28652, start_index=28501, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=RNA%20category,at%20protein%20level%20Protein%20expression')
77. AnnotationURLCitation(end_index=28862, start_index=28742, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=normal%20tissue,i%7D%20%201')
78. AnnotationURLCitation(end_index=29246, start_index=29113, title='Expression of RASA4B in cancer - Summary - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000170667-RASA4B/cancer#:~:text=PROGNOSTIC%20SUMMARY,favorable%20%20%203')
79. AnnotationURLCitation(end_index=29555, start_index=29449, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
80. AnnotationURLCitation(end_index=29856, start_index=29750, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
81. AnnotationURLCitation(end_index=30081, start_index=29975, title='RASA4 gene information - The Human Protein Atlas', type='url_citation', url='https://www.proteinatlas.org/ENSG00000105808-RASA4/summary/gene#:~:text=GTPase,i')
82. AnnotationURLCitation(end_index=30599, start_index=30427, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=In%20unstimulated%20cells%2C%20CAPRI%20is,this%20membrane%20association%20activates%20the')
83. AnnotationURLCitation(end_index=30763, start_index=30600, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=match%20at%20L140%20to%20function,oscillates%20between%20the%20plasma%20membrane')
84. AnnotationURLCitation(end_index=31154, start_index=30996, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=In%20the%20present%20study%2C%20we,membrane%20in%20response%20to%20receptor')
85. AnnotationURLCitation(end_index=31276, start_index=31155, title='Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC394250/#:~:text=activity,to%20an%20increase%20in%20its')
86. AnnotationURLCitation(end_index=31691, start_index=31576, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=Fc%20receptor%20%28FcR%29,These')
87. AnnotationURLCitation(end_index=32048, start_index=31933, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=Fc%20receptor%20%28FcR%29,These')
88. AnnotationURLCitation(end_index=32324, start_index=32174, title='A critical role for the Calcium-promoted Ras Inactivator in Fcγ receptor-mediated phagocytosis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC1464573/#:~:text=phagocytosis.%20CAPRI,essential%20for%20innate%20immune%20response')