TNFSF13B antibody
- Known as:
- TNFSF13B (anti-)
- Catalog number:
- orb48008
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- TNFSF13B antibody
Related genes to: TNFSF13B antibody
- Gene:
- TNFSF13B NIH gene
- Name:
- TNF superfamily member 13b
- Previous symbol:
- TNFSF20
- Synonyms:
- BAFF, THANK, BLYS, TALL-1, TALL1, CD257
- Chromosome:
- 13q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-19
- Date modifiied:
- 2018-11-22
Related products to: TNFSF13B antibody
Related articles to: TNFSF13B antibody
- Delayed graft function after kidney transplant is associated with increased acute rejection rates and poorer long-term outcomes. It is significantly more prevalent in recipients of deceased than living donor kidneys due to increased ischemia-reperfusion injury associated with prolonged warm and cold ischemic times. Although specific immune populations are associated with ischemia-reperfusion injury and delayed graft function, the precise cellular circuits distinguishing deceased from living donor transplants, as well as the donor and recipient-derived immune programs involved in early immunological responses, have not been defined at cellular resolution. - Source: PubMed
Publication date: 2026/09/22
Mak Martin LMurphy Julia MMathews Jessica ASu ShenghuiKonvalinka AnaEpelman SlavaCrome Sarah Q - BAFF and APRIL are TNF superfamily proteins that bind to BAFFR, TACI and BCMA, members of the TNF receptor superfamily. These proteins have both unique and overlapping roles in B cell development and survival and are major therapeutic targets for antibody- and B-cell-driven pathologies. BAFF and BAFFR are required for development and survival of follicular and marginal zone (MZ) B cells, whereas BAFF and APRIL acting through TACI and BCMA support plasma cell survival. TACI and BCMA can both be cleaved to generate soluble decoy receptors binding to BAFF or APRIL, forming feedback circuits. Thus, loss of TACI leads to an increase in BAFF, resulting in B cell hyperplasia. Recent work showed that TACI is required for MZ B cell development, a finding that has implications for understanding immune dysfunction in humans. Both monoallelic and biallelic loss-of-function TACI mutations result in immunodeficiency, potentially due to impaired MZ B cell function. Paradoxically, monoallelic TACI mutations predispose to autoimmunity. We propose this may be due to increased BAFF levels which promote selection of self-reactive B cell clones into the mature B cell pool, particularly the MZ B cell compartment. A deeper understanding of this ligand-receptor system is essential for effective therapeutic targeting. - Source: PubMed
Luff Daisy HSchweighoffer EdinaTybulewicz Victor L J - Down syndrome (DS), the most prevalent chromosomal disorder caused by trisomy 21, manifests intellectual disability and cognitive dysfunction. Cumulative studies confirm epigenetic pathways including DNA methylation and non-coding RNAs drive DS pathological progression. Histone post-translational modifications (PTMs) are core epigenetic regulators of fetal brain development. However, genome-wide PTM alterations and their downstream functions in fetal DS brains remain poorly characterized, leaving a key gap in revealing epigenetic mechanisms underlying DS neurodevelopmental defects. To address this, we aimed to establish the first comprehensive landscape of histone PTMs in fetal DS cortex and investigate whether specific PTM changes contribute to aberrant neurodevelopmental gene expression. - Source: PubMed
Publication date: 2026/07/30
Ye ShuaiBai BaolingZhao ZhuranWang LiMu QingZhang YangWang XinjuanZhang TingYu WeidongGuo Jingzhu - Acute inflammatory relapses in primary CNS demyelinating diseases, including relapsing multiple sclerosis (RMS), MOG-antibody-associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD), drive hospitalization, disability, and socioeconomic burden. Blood-based biomarkers are increasingly used for relapse detection and treatment monitoring. - Source: PubMed
Publication date: 2026/09/07
Chumakova Anastasia PDemetriou MichaelSy Michael - Persistent minimal residual disease (MRD) significantly contributes to chemotherapy resistance and relapse in pediatric B-cell acute lymphoblastic leukemia (B-ALL), with conventional clinical risk factors insufficiently explaining the variability in patient prognoses. This study sought to explore potential mechanisms linked to sustained MRD by integrating analyses of clinical cohorts with single-cell transcriptomics, aiming to identify reliable biomarkers for risk stratification and targeted therapy. - Source: PubMed
Publication date: 2026/08/18
Zhang LinlinLiu XiaoyangChen FangXu GangFan Yang