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Retinol-binding protein

Retinol-binding proteins (RBPs) are a family of carrier proteins that bind and transport , the biologically active form of . The form, retinol-binding protein 4 (RBP4), also known as serum retinol-binding protein, is a 21 kDa protein that functions as the principal carrier of in the bloodstream, ensuring its safe transport from the liver to peripheral tissues. Composed of a single polypeptide chain of 183 , RBP4 features a characteristic lipocalin fold with a β-barrel structure that accommodates one of in a non-covalent, high-affinity , protected from oxidation during circulation. To prevent rapid renal clearance, RBP4 forms a stable complex with (TTR), a larger thyroxine-binding protein, allowing delivery to target cells via specific membrane receptors such as stimulated by 6 (STRA6). First identified in 1968 through studies using radiolabeled in human , RBP4 circulates at concentrations of approximately 2–3 µM in healthy adults and plays a critical role in maintaining , which is essential for , immune function, embryonic development, and . Beyond its transport role, RBP4 has been implicated in broader physiological processes, including potential signaling functions independent of retinol binding, such as modulation of insulin sensitivity and in adipose and muscle tissues. Elevated levels of RBP4 are associated with conditions like , , and , where it may act as an contributing to , while deficiencies can lead to impaired delivery and symptoms such as night blindness. Structurally, the protein's eight-stranded β-barrel, flanked by an N-terminal coil and C-terminal α-helix, not only shields but also enables interactions with TTR and cellular uptake mechanisms, highlighting its evolutionary adaptation as a member of the lipocalin superfamily. continues to explore RBP4's therapeutic potential, including inhibitors targeting STRA6 for retinoid-related disorders like age-related .

Types of retinol-binding proteins

Plasma retinol-binding protein (RBP4)

Plasma retinol-binding protein 4 (RBP4) serves as the primary carrier for , the alcohol form of , in the bloodstream. It is predominantly synthesized in the liver by hepatocytes, where it facilitates the mobilization of from hepatic stores to peripheral tissues. The human RBP4 protein circulates as a mature polypeptide of 183 with a of approximately 21 . In circulation, RBP4 binds in a 1:1 stoichiometric ratio to form holo-RBP4, which then associates with (TTR) in a 1:1:1 complex. This complexation increases the overall molecular size, preventing glomerular in the kidneys and minimizing renal loss of the relatively small RBP4 molecule. In contrast, unbound apo-RBP4 (lacking retinol) is rapidly filtered by the glomeruli, reabsorbed in the proximal tubules, and cleared through , ensuring that free RBP4 does not accumulate in . Hepatic secretion of RBP4 is tightly regulated and dependent on retinol availability; holo-RBP4 is efficiently released into the bloodstream, while apo-RBP4 is largely retained intracellularly within hepatocytes when retinol is scarce. This mechanism maintains plasma homeostasis by coupling RBP4 export to the presence of its .

Cellular retinol-binding proteins (CRBPs)

Cellular retinol-binding proteins (CRBPs) are a family of intracellular proteins that specifically bind and all-trans-retinal with high , typically exhibiting dissociation constants (Kd) around 10^{-9} M, such as 3 nM for all-trans- binding to CRBP-I. These proteins protect bound retinoids from oxidation and non-specific metabolism while directing them to appropriate enzymes for further processing, including conversion to retinyl esters via :retinol acyltransferase (LRAT) or to via retinol dehydrogenases (RDH). By facilitating intracellular transport, storage, and metabolic channeling, CRBPs maintain retinoid homeostasis essential for , , and . The CRBP family comprises four subtypes—CRBP-I, CRBP-II, CRBP-III, and CRBP-IV—each with distinct tissue distributions and specialized roles in retinol handling. CRBP-I is the most ubiquitous isoform, prominently expressed in the liver, , and testis, where it supports retinol storage and metabolism across multiple tissues by enhancing esterification and directing substrates to retinoid-metabolizing enzymes. In contrast, CRBP-II is intestine-specific, highly concentrated in enterocytes where it constitutes approximately 1% of soluble protein, and plays a key role in facilitating dietary retinol absorption through efficient esterification and uptake. CRBP-III and CRBP-IV represent less common variants with more restricted functions and distributions. CRBP-III is expressed in the heart, , and epididymal (with no direct ortholog identified), contributing to retinyl ester incorporation into and supporting local utilization in these tissues. CRBP-IV, primarily found in the and liver in humans, has a less defined role but shares structural similarities that suggest involvement in binding and protection. Overall, these subtypes ensure tissue-specific retinol management, taking over from plasma RBP4 upon cellular uptake to orchestrate intracellular trafficking.
SubtypePrimary Expression SitesKey Functions
CRBP-ILiver, kidney, testis (ubiquitous)Retinol storage, metabolism, esterification
CRBP-IIIntestine (enterocytes)Retinol absorption, esterification
CRBP-IIIHeart, muscle, (human; no direct mouse ortholog)Retinyl ester incorporation (e.g., into )
CRBP-IV, liver (human)Retinoid binding (role unclear)

Cellular retinoic acid-binding proteins (CRABPs)

Cellular retinoic acid-binding proteins (CRABPs) are a family of intracellular lipid-binding proteins that specifically bind , the active metabolite of , to regulate its intracellular transport and bioavailability. The two primary isoforms, CRABP-I and CRABP-II, exhibit distinct expression patterns and functions in modulating retinoic acid signaling. CRABP-I is predominantly expressed in embryonic tissues such as the developing , craniofacial regions, and limb buds, as well as in adult and various other tissues including epidermal melanocytes. In contrast, CRABP-II is mainly found in differentiating epithelia, with high expression in the human epidermis, particularly in fibroblasts and suprabasal of the granular layer, and is largely restricted to the skin in adults. These proteins demonstrate high specificity for retinoic acid isomers, particularly all-trans- (ATRA), which they bind with subnanomolar affinity through a conserved hydrophobic pocket formed by β-barrel structures and α-helices. CRABPs function primarily to chaperone ATRA intracellularly, facilitating its delivery to retinoic acid receptors (RARs) and thereby regulating transcription essential for , , and embryonic . While both isoforms contribute to retinoid homeostasis, CRABP-I primarily sequesters ATRA in the cytoplasm, buffering its levels and promoting its degradation via enzymes to prevent excessive signaling. Conversely, CRABP-II enhances signaling by actively transporting ATRA to RARs and RXRs in the nucleus, supporting genomic pathways that influence and . CRABP-I and CRABP-II are encoded by distinct genes, CRABP1 and CRABP2, respectively, located on different chromosomes and exhibiting non-overlapping regulatory elements that drive their tissue-specific expression. studies in mice have elucidated their physiological roles: CRABP1-null mice develop normally without defects in limb or integrity, indicating that CRABP-I is dispensable for core signaling under physiological conditions. In comparison, CRABP2 results in impaired , including epidermal thinning, reduced and , diminished dermal thickness, and decreased , underscoring CRABP-II's critical involvement in epithelial maintenance and development.

Molecular structure

Overall protein fold

Retinol-binding proteins (RBPs) belong to the lipocalin superfamily, a group of small proteins specialized in binding and transporting hydrophobic ligands such as . The defining structural feature of this family is a conserved eight-stranded antiparallel β-barrel fold, where the β-strands are connected by loops to form a conical, hydrophobic cavity known as the calyx, which accommodates the nonpolar ligand. This architecture provides a stable enclosure for , protecting it from the aqueous environment while facilitating specific interactions. The β-barrel is stabilized by three bonds: Cys4–Cys160, Cys70–Cys174, and Cys120–Cys129, which contribute to the overall fold integrity. In human RBP4, the mature protein consists of 183 and lacks sites, remaining as a non-glycosylated polypeptide that enhances its and function in transport. These covalent linkages ensure the rigidity of the barrel, preventing ligand dissociation under physiological conditions. High-resolution crystal structures, such as that of holo-RBP4 in complex with (PDB ID: 1RBP), reveal the buried deep within the hydrophobic β-barrel, with its polyene chain aligned along the barrel axis and the β-ionone ring positioned at the closed end. The hydroxyl group at the 's terminal end remains partially exposed near the cavity entrance, enabling interactions with (TTR) in the plasma-bound complex. This positioning underscores the fold's role in balancing ligand sequestration and protein-protein recognition. While RBP4 has a sequence length of 183 , cellular retinol-binding proteins (CRBPs) exhibit a similar β-barrel fold but with shorter sequences of about 130-140 , reflecting their intracellular roles and adaptations for within cells. This conserved yet compact architecture across RBPs highlights the evolutionary optimization of the lipocalin fold for retinoid handling.

Retinol binding site and mechanism

Retinol binds non-covalently within the hydrophobic calyx of the β-barrel structure of retinol-binding proteins (RBPs), primarily through van der Waals and hydrophobic interactions with its polyene chain comprising four units. The β-ionone ring at one end of the molecule packs tightly against the ring of Trp20, contributing to the stability of the complex, while the hydroxyl group at the opposite end forms polar hydrogen bonds, including with the side chain of Glu90 and a coordinated molecule near the protein surface. These interactions position the retinol molecule linearly along the barrel axis, fully enclosed to shield it from the aqueous environment and prevent oxidation. The binding of to RBPs is high, with constants (Kd) typically in the range of 10^{-7} to 10^{-9} M, reflecting the physiological need for efficient solubilization and transport of this lipophilic . This is commonly measured using quenching assays, where binding quenches the intrinsic of the protein due to , allowing quantitative determination of binding and . For plasma RBP4, the holo-form (-bound) undergoes a conformational change that exposes a surface patch on loops C-D and E-F, enabling high- binding to (TTR) with a Kd of approximately 0.07 μM; this complex prevents glomerular filtration of the small RBP4 and facilitates targeted . In contrast, cellular retinol-binding proteins (CRBPs) channel bound to specific enzymes, such as :retinol acyltransferase (LRAT), promoting its esterification into retinyl esters for storage, through direct protein-protein interactions at the binding site entrance. RBPs exhibit specificity for retinol over , primarily due to mismatch of the polar end-group with the alcohol-coordinating residues in the pocket; while plasma RBP4 can accommodate with similar Kd to (~10^{-7} M), the charged group disrupts TTR complexation by altering the interface . Cellular CRBPs show even greater selectivity, with failing to bind effectively (no significant observed), as the pocket is optimized for the neutral hydroxyl group via residues like Gln108 and Lys40, preventing non-specific uptake of the more polar derivative. This discrimination ensures retinoids are directed to appropriate metabolic pathways without cross-talk.

Physiological function

Retinol transport and delivery

Dietary , primarily derived from retinyl esters and provitamin A , is absorbed in the by enterocytes after to free retinol by pancreatic and brush-border enzymes. Within enterocytes, cellular retinol-binding protein II (CRBP-II) binds the absorbed retinol with high affinity, facilitating its intracellular trafficking and directing it toward esterification by lecithin:retinol acyltransferase (LRAT) to form retinyl esters. These retinyl esters are then incorporated into nascent chylomicrons along with dietary and secreted into the for eventual delivery to the liver, where approximately 66-75% of circulating retinyl esters are cleared and stored predominantly in hepatic stellate cells as droplet-associated esters. In the liver, stored retinyl esters are hydrolyzed back to retinol by enzymes such as retinyl ester hydrolases, allowing retinol to bind apo-retinol-binding protein 4 (RBP4) synthesized in hepatocytes. The resulting holo-RBP4 (retinol-bound) forms a stable ternary complex with (TTR), a thyroxine-transporting protein, which prevents rapid renal filtration of the smaller RBP4 molecule and extends the plasma of the complex to approximately 11-16 hours. This holo-RBP4-TTR complex is secreted into the bloodstream, where RBP4 circulates at tightly regulated concentrations of 2-3 μM in healthy humans, ensuring steady-state delivery of retinol while maintaining vitamin A homeostasis despite fluctuations in dietary intake. Systemic delivery of to peripheral tissues occurs via the holo-RBP4-TTR complex docking at the STRA6 receptor, a expressed on the surface of target cells such as those in the eye, reproductive organs, and other vitamin A-dependent tissues. STRA6 acts as a bidirectional pore that catalyzes the release of from holo-RBP4 and its transfer to intracellular cellular retinol-binding proteins (CRBPs), such as CRBP-I, without requiring cellular energy; this process is reversible and can also facilitate efflux under conditions of excess intracellular stores. The TTR component modulates uptake efficiency by partially inhibiting STRA6 binding, providing regulatory control over tissue-specific retinol influx. To conserve vitamin A, the kidneys reabsorb over 99% of filtered apo- and holo-RBP4 via involving the megalin-cubilin complex on epithelial cells, recycling RBP4 back to the circulation and minimizing urinary loss. This efficient mechanism, combined with the stabilizing role of TTR, underscores the tightly controlled circulation of RBP4 to support equitable distribution while preventing toxicity from excess free .

Roles in retinoid metabolism and signaling

Cellular retinol-binding proteins (CRBPs) play a pivotal role in directing toward specific metabolic enzymes, ensuring efficient processing within cells. CRBP-I facilitates the presentation of retinol to retinyl ester hydrolases (REH) for of retinyl esters back to retinol, or to alcohol dehydrogenases (ADH) and retinol dehydrogenases (RDH) for oxidation to retinaldehyde, with saturable kinetics that enhance specificity. In contrast, CRBP-II primarily channels retinol to lecithin:retinol acyltransferase (LRAT) in intestinal cells for esterification and as retinyl esters, which are then incorporated into chylomicrons for systemic distribution; this process has a low Km (~0.7 μM) and limits biosynthesis to prioritize . Apo-CRBP-I further modulates these pathways by inhibiting formation and promoting , thereby regulating availability. Retinaldehyde generated from these oxidation steps is further metabolized to all-trans-retinoic acid (ATRA) by retinaldehyde dehydrogenases (RALDH1-3), serving as the primary ligand for signaling. ATRA is then bound by cellular retinoic acid-binding proteins (CRABPs), particularly CRABP-II, which delivers it to receptors () and retinoid X receptors (RXR) in the nucleus. This binding forms RAR/RXR heterodimers that interact with retinoic acid response elements (RAREs) in target gene promoters, activating transcription of developmental genes such as those in the Hox family, which are essential for embryonic patterning and . CRABP-I, meanwhile, directs ATRA toward catabolic pathways to fine-tune signaling intensity. Feedback mechanisms maintain homeostasis by inducing enzymes (CYP26A1, CYP26B1, CYP26C1) in response to excess or ATRA, promoting their degradation into polar metabolites. RBPs, including CRBPs and CRABPs, modulate substrate availability for these enzymes, preventing non-specific and ensuring retinoid scarcity is protected; for instance, CRBPs isolate to limit access to degradative pathways under normal conditions. Beyond vitamin A transport, retinol-binding protein 4 (RBP4) functions as an that influences systemic metabolism independently of delivery. Elevated circulating holo-RBP4 binds to its receptor STRA6 on adipocytes, triggering and activation of the JAK2-STAT5 signaling cascade. This pathway upregulates suppressor of signaling 3 (SOCS3), which inhibits and downstream signaling, thereby reducing insulin sensitivity and promoting accumulation. In , this mechanism contributes to , linking RBP4 to metabolic dysregulation. Recent studies as of 2025 have further elucidated RBP4's physiological roles in specialized tissues; for instance, brown fat-specific overexpression of RBP4 enhances adrenergic signaling to promote mobilization and oxidation in brown adipocytes. Additionally, RBP4 modulates mitochondrial function, inflammation, and in skeletal and , influencing and contractility. RBP4 also enhances cellular uptake, potentially impacting in various tissues.

Genetics and expression

Gene structure and chromosomal location

The human RBP4 gene, encoding plasma retinol-binding protein 4, is located on chromosome 10q23.33 and spans approximately 10 kb of genomic DNA with eight exons in its canonical transcript. The promoter region of RBP4 contains retinoic acid response elements (RAREs), consisting of two degenerate direct repeats that bind RAR/RXR heterodimers to mediate transcriptional regulation by retinoic acid. Genes for the cellular retinol-binding proteins exhibit similar compact structures: CRBP1 (RBP1) is situated on 3q23 and comprises six exons over about 22 kb, while CRBP2 (RBP2) maps to 3q23 with four exons. For the cellular retinoic acid-binding proteins, CRABP1 resides on 15q24.1 with four exons, and CRABP2 is located on 1q23.1, featuring five exons. Members of the retinol-binding protein family display high sequence conservation across vertebrate species, with identities often exceeding 80% among mammals and remaining substantial (around 60-70%) in more distant vertebrates such as and . is rare for these genes but has been observed in RBP4 across certain species, yielding minor transcript variants. Rare pathogenic variants in the RBP4 gene, such as the p.Gly75Asp , have been associated with phenotypes, including progressive retinal degeneration and .

Regulation of expression

The expression of retinol-binding protein 4 (RBP4) and cellular retinol-binding protein 1 (CRBP1) is transcriptionally upregulated by (RA) through its binding to retinoic acid receptors (RARs), which form heterodimers with retinoid X receptors (RXRs) to activate gene promoters and ensure homeostasis. This RA-mediated induction supports the intracellular and extracellular transport of , facilitating its conversion to RA for signaling. Additionally, the RBP4 promoter contains binding sites for hepatic nuclear factor 1α (HNF1α), a key that enhances hepatic expression of RBP4. Post-transcriptional regulation of RBP4 involves microRNAs (miRNAs) that target its mRNA, with dysregulation observed in metabolic conditions such as obesity, where altered miRNA profiles contribute to elevated RBP4 levels. Retinol availability also provides feedback regulation on retinoid-related gene expression, including stabilization mechanisms that maintain mRNA integrity under varying nutritional states, though direct effects on RBP4 mRNA stability require further elucidation in specific contexts. Tissue-specific expression of RBP4 is predominantly controlled in the liver by CCAAT/enhancer-binding protein (C/EBP) family members, which bind promoter elements to drive basal and inducible transcription during acute phase responses. In adipose tissue, RBP4 expression is upregulated under metabolic stress, such as in obesity, where it correlates with insulin resistance and altered lipid metabolism, independent of hepatic contributions. During embryogenesis, cellular retinoic acid-binding proteins (CRABPs) are upregulated by , such as Hoxb1, which act as transcriptional activators to establish spatially restricted expression domains, for instance in rhombomere 4 of the developing , thereby coordinating signaling with anterior-posterior patterning.

Role in reproduction

Synthesis and function during

During , hepatic synthesis of retinol-binding protein 4 (RBP4) increases to mobilize from liver stores, ensuring adequate supply for fetal development and growth. This upregulation is evident from early , with RBP4 levels rising progressively to support demands, as observed in studies of maternal circulation during the first and second trimesters. Higher RBP4 concentrations correlate positively with fetal size at birth, underscoring its role in promoting intrauterine growth independent of maternal factors. At the placental interface, the stimulated retinoic acid 6 (STRA6) receptor facilitates retinol uptake from circulating holo-RBP4 complexes into cells, enabling transplacental transfer to the . This receptor-mediated process is critical for directing recently ingested across the maternal-fetal barrier, with RBP4-bound retinol released and rebound to fetal RBP4 for distribution. Placental expression of retinoid-binding proteins, including RBP4, supports this vectorial transport, preventing direct crossover of maternal RBP4 while maintaining . Local synthesis of retinoid-binding proteins occurs in the and , where cellular retinol-binding protein 1 (CRBP1) and RBP4 are upregulated during to facilitate embryonic implantation in humans. Decidual stromal cells exhibit increased CRBP1 and retinol-metabolizing enzymes upon progesterone exposure, aiding production essential for invasion and uterine receptivity. Retinol deficiency, often reflected in low RBP levels, disrupts this process and is associated with neural tube defects due to impaired formation and closure. Retinol delivered via RBPs serves as a precursor for , which binds nuclear receptors to regulate expression, directing anterior-posterior patterning of limbs and organs during embryogenesis. This signaling establishes Hox boundaries critical for segmentation and morphogenesis, with disruptions leading to congenital malformations. In the , internalized retinol is metabolized to retinoic acid for local and fetal signaling, ensuring precise spatiotemporal control of developmental gradients. Imbalances in RBP-mediated retinol transport pose risks; low maternal levels, transported by RBP4, are associated with higher rates, likely due to inadequate support for implantation and early . Conversely, excess exposure, as with —a analog—exerts teratogenic effects, causing craniofacial, cardiac, and defects in up to 35% of exposed fetuses. Regulatory guidelines limit supplemental to 10,000 daily during to mitigate such risks.

Expression in livestock species

In livestock species, retinol-binding protein (RBP) expression during exhibits distinct patterns tailored to the reproductive of agricultural animals such as , sheep, and pigs. In bovines, endometrial RBP secretion increases during the and peaks around day 15 post-estrus, driven by progesterone sensitivity that modulates uterine epithelial cell activity to prepare for attachment. By day 13, RBP mRNA is strongly expressed in the trophectoderm of elongating blastocysts, facilitating local delivery essential for development and implantation. This temporal upregulation aligns with the progesterone-dominated , where RBP concentrations in uterine secretions rise to support early embryonic needs. In ovine and porcine species, RBP expression shifts toward extraembryonic tissues during mid-gestation. In sheep, RBP mRNA appears in the and areolar trophoblasts by days 20-45, coinciding with , while endometrial glands continue synthesis to enrich the uterine milieu with for fetal-maternal exchange. Similarly, in pigs, endometrial RBP production, localized to glandular , intensifies under progesterone influence around days 11-13 with elongation, extending to chorionic structures by day 20 to sustain nutrient transport. These patterns reflect adaptations to synepitheliochorial (ruminants) and epitheliochorial (pigs) , where RBP ensures availability during rapid proliferation. Functionally, RBP in supports implantation and by delivering to developing embryos, with deficiencies associated with embryonic loss in nutrient-restricted herds, particularly under low diets that impair uterine secretion. These differences underscore RBP's role in optimizing reproductive efficiency in agricultural contexts, akin to human pregnancy but adapted to extended al cycles in . Ruminants have greater dietary requirements due to ruminal microbial degradation, alongside consistent mRNA upregulation in early across to meet heightened demands.

Clinical significance

Use as a nutritional biomarker

Plasma -binding protein 4 (RBP4) concentration serves as a reliable indicator of status because it transports from the liver to peripheral tissues, reflecting hepatic stores under normal conditions. In healthy individuals, plasma RBP4 levels typically range from 10 to 50 μg/mL, with concentrations dropping below 15 μg/mL (equivalent to <0.7 μmol/L) signaling insufficiency, aligning with proposed cutoffs for deficiency assessment. This is particularly valuable in nutritional surveys, as low RBP4 levels are observed in conditions like and chronic illnesses due to impaired hepatic synthesis stemming from protein malnutrition. Unlike prealbumin, which is a negative acute-phase reactant, RBP4 concentrations remain relatively stable during acute , making it a preferable marker for evaluating nutritional status in such settings. In clinical and field assessments, immunoassays such as enzyme-linked immunosorbent assay () are commonly employed to quantify total RBP4, apo-RBP4 (unbound form), or holo-RBP4 (retinol-bound form), providing insights into both carrier availability and . These measurements correlate well with functional tests like the relative dose-response (RDR) or modified RDR, which detect low hepatic reserves by monitoring mobilization after an oral dose. Despite its utility, RBP4 as a has limitations, including influence from renal function; plasma levels are often elevated in due to reduced clearance, potentially masking true status. Additionally, concomitant can lower RBP4 concentrations, complicating interpretation in populations with overlapping deficiencies.

Associations with human diseases

Retinol-binding protein 4 (RBP4) has been implicated in the pathogenesis of metabolic syndrome, where elevated circulating levels are observed in individuals with obesity and type 2 diabetes, contributing to insulin resistance through mechanisms involving the STRA6 receptor. Studies indicate that plasma RBP4 concentrations are approximately 1.7- to 2-fold higher in patients with type 2 diabetes compared to nondiabetic controls, with adipose tissue serving as a primary source of this elevation. This dysregulation promotes systemic insulin resistance by activating STRA6 in tissues such as adipose and pancreatic beta cells, leading to impaired glucose uptake and beta-cell dysfunction. Mutations in the RBP4 gene are associated with retinal dystrophies, such as progressive retinal dystrophy with or without dysfunction, resulting from impaired retinol transport to the . These genetic variants disrupt the binding and delivery of retinol to and photoreceptors, leading to , visual field loss, and eventual severe vision impairment. For instance, specific homozygous or compound heterozygous mutations in RBP4 cause retinal dystrophy with iris and comedogenic syndrome (RDCCAS), characterized by early-onset and progressive photoreceptor degeneration due to deficient supply. High-dose supplementation has shown potential to ameliorate symptoms in some RBP4-related cases by enhancing alternative retinol uptake pathways. In cancer, particularly (), cellular retinoic acid-binding proteins (CRABPs) play a role in signaling dysregulation, with their upregulation influencing therapeutic responses to all-trans (ATRA). APL cells exhibit altered CRABP expression, which modulates the availability of for binding to (RARs), a pathway hijacked by the PML-RARα fusion protein. ATRA therapy exploits this by inducing differentiation of leukemic promyelocytes through restoration of RAR signaling, leading to remission in most patients; however, high CRABP levels in resistant cells can sequester and reduce efficacy. Seminal studies have established CRABPs as key regulators in this context, with their modulation enhancing ATRA's degradative effects on the oncogenic . RBP4 also serves as an inflammatory marker in non-alcoholic (NAFLD), where elevated hepatic expression correlates with and . In NAFLD patients, serum RBP4 levels are increased and associated with disease severity, promoting mitochondrial dysfunction and lipid accumulation in hepatocytes via retinol-independent pathways. Animal models demonstrate that RBP4 overexpression exacerbates hepatic buildup, while RBP4 mice exhibit improved glucose tolerance and insulin sensitivity, underscoring its role in metabolic beyond nutritional contexts.

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