SLC35A2 Antibody

What is the biological function of SLC35A2 protein?

SLC35A2 (Solute Carrier Family 35 Member A2) primarily functions as a UDP-galactose transporter that moves UDP-galactose from the cytosol into the Golgi apparatus. It operates as an antiporter, exchanging UDP-galactose primarily for UMP, though it can also exchange for AMP and CMP . Additionally, it can transport UDP-N-acetylgalactosamine (UDP-GalNAc) and other nucleotide sugars . As a provider of UDP-galactose to galactosyltransferases in the Golgi apparatus, SLC35A2 plays an essential role in globotriaosylceramide/globoside (Gb3Cer) synthesis from lactosylceramide . This transport function is critical for proper glycosylation of proteins and lipids, influencing numerous cellular processes.

What are the common alternative names for SLC35A2 in scientific literature?

When searching scientific databases and interpreting research papers, it's important to recognize all nomenclature variations for SLC35A2. The protein is also known as UGALT, UGT, UGTL, UDP-galactose translocator, and UDP-Gal-Tr . Using multiple search terms that include these alternative designations ensures comprehensive literature reviews and prevents overlooking relevant publications. This is particularly important when conducting systemic reviews or meta-analyses of SLC35A2-related research.

How is SLC35A2 expression regulated in normal cellular physiology?

SLC35A2 expression is tightly regulated in normal cells as part of the glycosylation machinery. Although the search results don't specifically detail all regulatory mechanisms, research indicates that SLC35A2 expression varies across tissue types and developmental stages. In pathological conditions, particularly cancer, SLC35A2 often shows dysregulated expression . Understanding normal regulatory pathways informs research on pathological changes. When designing experiments to study SLC35A2 regulation, researchers should include appropriate normal tissue controls alongside disease samples and consider time-course experiments to capture dynamic regulatory changes.

How does SLC35A2 influence cancer cell behavior at the molecular level?

Functional experiments have demonstrated that SLC35A2 silencing inhibits proliferation, migration, and invasion of breast cancer cells . The mechanistic investigation revealed that SLC35A2 affects the metastatic potential of cancer cells through modulation of the Wnt/β-catenin/EMT signaling pathway . This suggests SLC35A2's role extends beyond its canonical transport function to influence key oncogenic signaling pathways. When designing experiments to study SLC35A2's molecular functions in cancer, researchers should consider examining multiple downstream pathways and using both gain-of-function and loss-of-function approaches to comprehensively characterize its effects.

What is the relationship between SLC35A2 expression and immune infiltration in tumors?

Multiple algorithmic immune infiltration analyses have revealed an inverse relationship between SLC35A2 expression and infiltrating immune cells in various tumors . Specifically:

This negative association between SLC35A2 expression and lymphocyte infiltration suggests SLC35A2 may influence the tumor microenvironment and potentially affect immunotherapy responses . When studying SLC35A2 in the context of tumor immunity, researchers should employ multiple immune infiltration algorithms to ensure robust results.

What are the optimal experimental conditions for detecting SLC35A2 using antibody-based techniques?

For optimal detection of SLC35A2 using antibody-based techniques such as Western blotting, researchers should consider using a dilution ratio of 1/2000 for the SLC35A2 antibody . Validated antibodies, such as rabbit polyclonal antibodies corresponding to recombinant fragment protein within Human SLC35A2 (amino acids 100-250), have been shown to be effective . When designing experiments, include positive controls (tissues or cell lines known to express SLC35A2) and negative controls (SLC35A2 knockout or knockdown samples). For immunohistochemistry applications, optimize antigen retrieval methods and validate antibody specificity through appropriate controls.

How should researchers design gene silencing experiments to study SLC35A2 function?

When designing gene silencing experiments to study SLC35A2 function, researchers should consider using multiple siRNA or shRNA constructs targeting different regions of the SLC35A2 transcript to avoid off-target effects. Based on published successful approaches, functional assays to assess the impact of SLC35A2 silencing should include cell proliferation, invasion, and migration assays . Additionally, researchers should examine the effects on the Wnt/β-catenin/EMT signaling pathway, as this has been identified as a key downstream mechanism affected by SLC35A2 . To ensure comprehensive analysis, both in vitro experiments with cell lines and in vivo models should be considered, particularly for cancer-related studies.

What considerations are important when developing a prognostic model incorporating SLC35A2 expression?

• Use multivariate Cox regression analysis to confirm SLC35A2 as an independent prognostic factor

• Test the model across different patient cohorts to ensure generalizability

• Consider integrating SLC35A2 with other molecular markers for improved prognostic accuracy

• Validate findings using both RNA sequencing data and protein expression data

This comprehensive approach ensures robust prognostic models with clinical utility.

How can SLC35A2 expression be used to predict immunotherapy response?

SLC35A2 expression has shown significant predictive value for immunotherapy response in patients with diverse cancers . Analysis of four independent immunotherapy cohorts revealed that SLC35A2 expression was higher in patients exhibiting complete and partial immune checkpoint blockade (ICB) responses than in those exhibiting stable and progressive disease . The Tumor Immune Dysfunction and Exclusion (TIDE) score, which is widely accepted for assessing immune response, showed a negative correlation with SLC35A2 expression in 20 tumor types . This suggests individuals with high SLC35A2 expression may have reduced immune evasion and potentially better responses to immunotherapy.

A methodological approach to using SLC35A2 as an immunotherapy response predictor should include:

• Quantification of SLC35A2 expression using standardized methods (qPCR, RNA-seq, or IHC)

• Integration with other established predictive biomarkers (PD-L1 expression, TMB, MSI)

• Correlation with TIDE scores

• Validation in independent cohorts before clinical implementation

What is the relationship between SLC35A2 expression and tumor mutational burden (TMB) or microsatellite instability (MSI)?

SLC35A2 expression shows significant correlations with both tumor mutational burden (TMB) and microsatellite instability (MSI) across multiple cancer types . These correlations vary by cancer type, with some showing positive and others showing negative relationships. The significance of these correlations (p < 0.05 to p < 0.001) indicates they are not random associations .

When investigating these relationships, researchers should:

• Analyze both TMB and MSI alongside SLC35A2 expression

• Use Spearman's correlation analysis for non-parametric assessment

• Stratify analyses by cancer type rather than pooling all cancers together

• Consider these relationships when interpreting SLC35A2's role in predicting immunotherapy response

Understanding these correlations helps contextualize SLC35A2's potential as a biomarker in the evolving landscape of precision oncology.

How does SLC35A2 influence the cancer immune cycle?

SLC35A2 appears to influence multiple steps of the cancer immune cycle, which includes antigen release, presentation, T-cell priming, trafficking, infiltration, and cancer cell killing. Single-sample gene set enrichment analysis (ssGSEA) has demonstrated that SLC35A2 expression in multiple cancers (PAAD, READ, SKCM, STAD, CESC, LUAD, COAD, LUSC, and HNSC) is negatively related to immune cell infiltration levels .

Furthermore, when SLC35A2 expression is low in certain cancers (LUSC, COAD, HNSC, and LUAD), multiple steps of the immune response are activated . This suggests SLC35A2 may act as an immunosuppressive factor in these cancer types. When researching SLC35A2's influence on cancer immunity, a comprehensive approach should include:

• Analysis of all immune cycle steps rather than focusing on a single component

• Comparison between high and low SLC35A2 expression groups using robust statistical methods

• Validation of computational findings with experimental models

• Integration of spatial information about immune cell distribution relative to SLC35A2-expressing cells

How can researchers address the cellular heterogeneity issue when studying SLC35A2 in tumor samples?

When studying SLC35A2 in tumor samples, addressing cellular heterogeneity is crucial for accurate interpretation. Current limitations acknowledged in the literature note that microarray and sequencing data extracted from tumor tissues may introduce systematic bias at the cellular level . To overcome this limitation, researchers are advised to employ single-cell RNA sequencing in future studies .

A methodological approach to address heterogeneity should include:

• Microdissection techniques to isolate specific tumor regions

• Single-cell analysis approaches (scRNA-seq, CyTOF, single-cell Western blotting)

• Spatial transcriptomics to preserve positional information

• Validation of bulk findings in purified cell populations

• Analysis of SLC35A2 expression in different cellular compartments (tumor cells, immune cells, stromal cells)

These approaches help deconvolute the complex cellular milieu of tumors and provide more accurate insights into SLC35A2's role in specific cell types.

What are the critical controls needed when validating new SLC35A2 antibodies?

When validating new SLC35A2 antibodies for research use, several critical controls are essential to ensure specificity and reproducibility:

• Positive controls: Use samples with confirmed SLC35A2 expression (validated cell lines or tissues)

• Negative controls: Include SLC35A2 knockout/knockdown samples or tissues known not to express SLC35A2

• Peptide competition: Pre-incubation with the immunizing peptide should eliminate specific signals

• Multiple detection methods: Validate findings using orthogonal techniques (Western blot, IHC, IF, ELISA)

• Cross-reactivity assessment: Test against closely related proteins, particularly other SLC35 family members

• Isotype controls: Include appropriate isotype-matched control antibodies

• Species validation: Verify reactivity across relevant species (human and mouse have been confirmed for some antibodies)

Thorough validation ensures experimental results accurately reflect SLC35A2 biology rather than artifacts of non-specific antibody binding.

What are promising future directions for SLC35A2 research in cancer and immunotherapy?

Several promising future directions for SLC35A2 research emerge from current findings:

• Mechanistic studies: Further elucidate the underlying mechanisms of SLC35A2 in cancer progression, metastasis, and immunity beyond the currently identified Wnt/β-catenin/EMT pathway

• Therapeutic targeting: Explore the potential of targeting SLC35A2 therapeutically, particularly in combination with immunotherapy. Molecular docking studies have already identified compounds like vismodegib and abiraterone that may interact with SLC35A2

• Biomarker validation: Validate SLC35A2 as a predictive biomarker for immunotherapy response in prospective clinical trials, particularly for LUAD, LUSC, SKCM, and BLCA where preliminary evidence shows promise

• Single-cell analysis: Apply single-cell technologies to understand SLC35A2's role in different cell populations within the tumor microenvironment

• Glycosylation studies: Investigate how SLC35A2-mediated changes in glycosylation patterns affect tumor cell behavior and immune recognition

Researchers pursuing these directions should employ multidisciplinary approaches combining computational, molecular, cellular, and clinical methodologies to comprehensively advance our understanding of SLC35A2's role in human disease.