CECR1 Blocking Peptide
- Known as:
- CECR1 Blocking Peptide
- Catalog number:
- 33r-6325
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CECR1 Blocking Peptide
Related genes to: CECR1 Blocking Peptide
- Gene:
- ADA2 NIH gene
- Name:
- adenosine deaminase 2
- Previous symbol:
- IDGFL, CECR1
- Synonyms:
- ADGF
- Chromosome:
- 22q11.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2019-04-23
Related products to: CECR1 Blocking Peptide
Related articles to: CECR1 Blocking Peptide
- The COVID-19 pandemic has highlighted the importance of understanding immune regulation underlying disease severity. Adenosine deaminase (ADA), an enzyme with ADA1 and ADA2 isoforms, modulates immune responses and is mainly expressed in lymphoid tissues. This study examined ADA activity and its relationship with macrophage polarization in COVID-19. - Source: PubMed
Publication date: 2026/05/04
Bozkurt TugceSimsek AbdurrahmanKizmaz Muhammed AliCagan ErenKose HulyaIskin Ali ErenPayaslioğlu Ayse MeldaKaradag MehmetAkalin Emin HalisKilic Sara SebnemBudak Ferah - Deficiency of adenosine deaminase 2 (DADA2) is caused by mutations in the ADA2 gene and results in an auto-inflammatory state. Hepatosplenomegaly, with or without abnormalities in liver enzymes, has been reported in DADA2. Anti-tumour necrosis factor (anti-TNF) therapy is the standard of care for the prevention of recurrent ischemic strokes and reduction of inflammatory burden. However, little is known about the extent of hepatic involvement and the utility of non-invasive tools for identifying liver disease and monitoring treatment response. - Source: PubMed
Shaik Mohammed RifatAlao HawwaShaik Nishat AnjumKapuria DevikaGopalakrishna HarishHan Ma Ai ThandaTakyar VarunHoffmann PatrycjaStone DeborahWilson LorenaVidegar-Laird RyanRedd BernadetteKleiner David EKoh ChristopherKastner Daniel LDimitrova DimanaOmbrello Amanda KHeller Theo - Deficiency of adenosine deaminase 2 (DADA2) is a rare monogenic autoinflammatory vasculopathy characterised by systemic vasculitis, immune dysregulation and haematological abnormalities. We report a man in his 30s who presented with recurrent ischaemic strokes, cytopenias, renal microaneurysms, cardiomyopathy and gastrointestinal involvement. He was initially diagnosed with polyarteritis nodosa and treated with conventional immunosuppression, with poor clinical response. Genetic testing confirmed DADA2, following which infliximab therapy was initiated, resulting in clinical stabilisation and improvement in inflammatory and haematological parameters, with stabilisation of cardiac function. This case highlights the importance of early genetic diagnosis and timely initiation of tumour necrosis factor inhibitor therapy to prevent irreversible organ damage. - Source: PubMed
Publication date: 2026/04/29
Muniraju TejasSankaralingam RajeswariRamesh Prabhu NidhiMohmmed Ashraf Memon SharminTejaswi Kottu Lakshmi - Deficiency of adenosine deaminase 2 (DADA2) is a rare autosomal recessive autoinflammatory disorder manifesting with variable clinical features, including systemic inflammation, vasculopathy, and recurrent ischemic or hemorrhagic strokes. Recurrent strokes have been well-established as part of the spectrum of DADA2 in keeping with the presentation of our patient. However, movement disorders in DADA2 have not been well-described. We report a case presenting with childhood-onset recurrent febrile illness, recurrent ischemic strokes, progressive generalized dystonia, intellectual disability and vasculitic rash. Neuroimaging revealed old pontine and bilateral thalamic infarcts while blood investigations revealed elevated inflammatory markers, pancytopenia and immunodeficiency. This case highlights the importance of recognizing DADA2 as a potentially treatable cause of early-onset stroke and movement disorder, emphasizing the need for timely diagnosis and targeted therapy. - Source: PubMed
Publication date: 2026/04/24
Lim Thien ThienPor Chia YinTeh Chee MingKoay Beng Siang - Cutaneous leishmaniasis (CL) caused by Leishmania braziliensis is characterized by intense inflammation that contributes both to parasite control and tissue pathology. Purinergic signalling, particularly mediated by adenosine and its receptors, has been implicated in immune modulation during Leishmania infection, yet its functional relevance in L. braziliensis remains poorly defined. Here, we investigated the roles of adenosine A2A and A2B receptors and adenosine deaminase (ADA) in regulating immune responses during L. braziliensis infection. Transcriptomic analyses of human CL lesions revealed increased expression of ADORA2A, which paradoxically correlated positively with pro-inflammatory and microbicidal gene signatures. Despite modulating the receptor expression on L. braziliensis-infected macrophages as well, pharmacological inhibition of A2A or A2B receptors did not affect parasite burden, reactive oxygen species (ROS) production, or inflammatory cytokine release. Thus suggesting that adenosine receptor signalling is dispensable in this context. In contrast, ADA and ADA2 were markedly upregulated in CL lesions and infected macrophages and showed strong positive correlations with inflammatory mediators. Functional inhibition of ADA with pentostatin significantly increased intracellular parasite load and reduced ROS, TNF-α, and IL-1β production, demonstrating a critical role for ADA in sustaining macrophage microbicidal activity. These findings suggest that ADA activity is central to modulating adenosine-mediated immunosuppression in CL and may serve as both a biomarker of disease activity and a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/19
de Paula Wesley Limade Oliveira Geovanna MedeirosRibeiro-Dias FátimaGomes Rodrigo Saar