Pages that link to "Q40485228"
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The following pages link to Dual antigen recognition by B cells (Q40485228):
Displaying 34 items.
- Association of four antigens of the tetraspans family (CD37, CD53, TAPA-1, and R2/C33) with MHC class II glycoproteins (Q28250176) (← links)
- The CD19 signal transduction molecule is a response regulator of B-lymphocyte differentiation (Q33707690) (← links)
- CD81 gene defect in humans disrupts CD19 complex formation and leads to antibody deficiency (Q33755327) (← links)
- CD19 is a central response regulator of B lymphocyte signaling thresholds governing autoimmunity (Q33826028) (← links)
- Natural antibodies and complement link innate and acquired immunity (Q34103323) (← links)
- Studies of the humoral immune response (Q34242639) (← links)
- CD19 regulates intrinsic B lymphocyte signal transduction and activation through a novel mechanism of processive amplification (Q34242679) (← links)
- Neutralizing antiviral antibody responses (Q34419527) (← links)
- CD19, CD21, and CD22: multifaceted response regulators of B lymphocyte signal transduction (Q34577064) (← links)
- Entry of Francisella tularensis into Murine B Cells: The Role of B Cell Receptors and Complement Receptors (Q35687639) (← links)
- Discordant expression of immunoglobulin and its associated molecule mb-1/CD79a is frequently found in mediastinal large B cell lymphomas. (Q35794900) (← links)
- Complement C4 inhibits systemic autoimmunity through a mechanism independent of complement receptors CR1 and CR2 (Q36369080) (← links)
- Protective T cell-independent antiviral antibody responses are dependent on complement (Q36375462) (← links)
- Antiviral antibody responses: the two extremes of a wide spectrum (Q36405084) (← links)
- Tissue-specific expression of the human CD19 gene in transgenic mice inhibits antigen-independent B-lymphocyte development. (Q36654682) (← links)
- Antiviral protection and germinal center formation, but impaired B cell memory in the absence of CD19. (Q36851746) (← links)
- New frontiers of primary antibody deficiencies. (Q37951367) (← links)
- Follicular Dendritic Cells: Origin and Function (Q40431523) (← links)
- Signal transduction by the antigen receptors of B and T lymphocytes. (Q40500421) (← links)
- Alteration of B-cell antigen receptor signaling by CD19 co-ligation. A study with bispecific antibodies. (Q41168330) (← links)
- Hematopoietic cell phosphatase is recruited to CD22 following B cell antigen receptor ligation. (Q41302172) (← links)
- The CD19-CD21 complex regulates signal transduction thresholds governing humoral immunity and autoimmunity (Q41360894) (← links)
- The phosphoprotein phosphatase calcineurin controls calcium-dependent apoptosis in B cell lines (Q41489248) (← links)
- Animal membrane receptors and adhesive molecules (Q41506599) (← links)
- Linkages of innate and adaptive immunity (Q41729800) (← links)
- Complement receptors regulate differentiation of bone marrow plasma cell precursors expressing transcription factors Blimp-1 and XBP-1 (Q41871689) (← links)
- Reduced CD19 expression and decreased memory B cell numbers in transient hypogammaglobulinemia of infancy (Q43493905) (← links)
- Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection (Q45733086) (← links)
- Checkpoints of B cell differentiation: visualizing Ig-centric processes. (Q50973728) (← links)
- Impairment of T-cell-dependent B-cell responses and B-1 cell development in CD19-deficient mice. (Q52052343) (← links)
- B cell antigen receptor cross-linking induces tyrosine phosphorylation and membrane translocation of a multimeric Shc complex that is augmented by CD19 co-ligation (Q61863581) (← links)
- Novel mutations in a Japanese patient with CD19 deficiency (Q63804793) (← links)
- Detection of two variants of complement component C3 in C3-deficient guinea pigs distinguished by the absence and presence of a thiolester (Q73179229) (← links)
- Beyond monogenetic rare variants: tackling the low rate of genetic diagnoses in predominantly antibody deficiency (Q98499845) (← links)