Camp Responsive Element Binding Protein
- Known as:
- Camp Responsive Element Binding Protein
- Catalog number:
- RP17130730010
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- Camp Responsive Element Binding Protein
Ask about this productRelated genes to: Camp Responsive Element Binding Protein
- Gene:
- CAMP NIH gene
- Name:
- cathelicidin antimicrobial peptide
- Previous symbol:
- -
- Synonyms:
- CAP18, FALL39, FALL-39, LL37
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-12
- Date modifiied:
- 2016-10-05
Related products to: Camp Responsive Element Binding Protein
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody"Affordable Gel Doc System with UV, Epi white & white
backlight Source for fluorescencent dye-stained DNA (ex.
EtBr)/protein (ex. SYPRO Ruby) gel imaging""Recombinant Human Palmitoyl-protein thioesterase 1_PPT1""Recombinant Human Palmitoyl-protein thioesterase 1_PPT1""Recombinant Human Palmitoyl-protein thioesterase 1_PPT1""Recombinant Human Palmitoyl-protein thioesterase 1_PPT1""Recombinant Human Regenerating islet-derived protein 4_REG4""Recombinant Human Regenerating islet-derived protein 4_REG4""Recombinant Human Regenerating islet-derived protein 4_REG4""Recombinant Human Regenerating islet-derived protein 4_REG4"((Cys31,Nva34)_Neuropeptide Y (27_36))2 Salt _ Binding (Disulfide_bond) Synonym SumFormula C116H186N36O28S2((Cys31,Nva34)_Neuropeptide Y (27_36))2 Salt _ Binding (Disulfide_bond) Synonym SumFormula C116H186N36O28S2(1_Adamantaneacetyl1,D_Tyr(Et)2,Val4,Abu6, Arg8·9)_Vasopressin Salt _ Binding _ Synonym SumFormula C62H94N16O11(1_Adamantaneacetyl1,D_Tyr(Et)2,Val4,Abu6, Arg8·9)_Vasopressin Salt _ Binding _ Synonym SumFormula C62H94N16O11(1_Adamantaneacetyl_D_Arg0,Hyp3,b_(2_thienyl)_Ala5·8,D_Phe7)_Bradykinin Salt _ Binding _ Synonym SumFormula C68H99N19O14S2 Related articles to: Camp Responsive Element Binding Protein
- Obesity is a major global public health concern closely linked to the development and progression of various gynaecological disorders, particularly polycystic ovary syndrome (PCOS) and endometrial cancer. Incretins, a group of gut-derived hormones primarily including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are widely recognised for their roles in glycemic control and insulin secretion. Accumulating evidence reveals that GLP-1 and GIP also participate in modulating inflammation, autophagy, immune response and gut-brain communication through multiple signalling pathways, thereby playing important roles in female reproductive disorders. This review provides a comprehensive overview of the mechanisms and therapeutic potential of incretins in gynaecological conditions. - Source: PubMed
Yan JiayuCao MinyueDing YanZhang YiqinSun YihanJiang GenyiZhang YanliKang LuyaoZhou XueLuo JingLi Bilan - Endothelial dysfunction is a hallmark of pathological angiogenesis and associated with erythrocyte extravasation and lysis. Whether mediators released from lysed erythrocytes instruct endothelial cells (ECs) for new vessel formation is unknown. Here, we show that the membrane fraction of lysed erythrocytes activates inflammatory endothelial gene transcription and metabolically reprograms ECs to promote angiogenic sprout formation. Alterations in endothelial glucose metabolism occurred downstream of NFκB p65 activation by extracellular ATP via fast-acting endothelial P2X7 receptors and also involved ATP-mediated adenylyl cyclase activation and cyclic AMP generation via P2RY11. Overexpression and acetylation of histone 3 at lysine 27 of NR4A1 was identified as anti-inflammatory control mechanism and angio-metabolic switch activating VEGF, PFKFB3 and other AP-1 dependent gene transcription programs. The angiogenic potential of lysed erythrocyte membranes from patients with peripheral artery disease was impaired and could be restored by inhibiting endothelial phosphodiesterase 4 to prevent endothelial cAMP degradation. Our findings uncover that erythrolysis metabolically primes ECs for angiogenesis and that targeting endothelial cAMP generation may be a promising strategy to restore endothelial angiogenic functions. - Source: PubMed
Publication date: 2026/09/25
Gogiraju RajinikanthMoiko KaterynaBochenek Magdalena LGreulich FranziskaWitzler ClaudiusSchmitz WernerZifkos KonstantinosDerieux CécileGhasemi ImanGuliani PayalSun BeichenEspinola-Klein ChristineUhlenhaut Henriette NBock AndreasRuf WolframMadhusudhan ThatiLurz PhilippSchäfer Katrin - To systematically characterize the epitranscriptomic landscape of N-methyladenosine (mA) methylation in major depressive disorder (MDD) and elucidate its functional consequences on mRNA and lncRNA regulation. - Source: PubMed
Publication date: 2026/09/11
Liu LiangYang ZhaonanTan KunruXu ShuhaoXu JiaNiu JinbaoYang Xiuxian - Neonatal alloimmune thrombocytopenia (NAIT) can present as severe thrombocytopenia in an otherwise healthy neonate and may lead to serious bleeding, intracranial hemorrhage, and even death. This report presents two siblings affected by NAIT. The first sibling was diagnosed when the infant presented after birth with petechial hemorrhages and a profoundly low platelet count. During the subsequent pregnancy, the mother was treated with a protocol of IVIG and steroid. This resulted in a higher platelet count at birth in the second sibling, although still severely thrombocytopenic, without physical signs or symptoms of thrombocytopenia. In this case, the infant responded rapidly to an antigen-matched platelet transfusion. This case series calls attention to the importance of close follow-up and optimum management of NAIT. - Source: PubMed
Publication date: 2026/09/24
Abedin NaheedAbdulkader AhmadNguyen TiffanyRanasaria Mansi - Renal cell carcinomas (RCC) comprise multiple molecularly distinct cancers but most are treated empirically with therapies designed for clear cell RCC (ccRCC), the most common subtype, due to incomplete understanding of subtype-specific biology. We analyzed single-cell transcriptomes and chromatin accessibility profiles from translocation renal cell carcinoma (tRCC), an aggressive RCC defined by oncogenic TFE3 gene fusions. We show that, despite arising from a proximal tubule cell of origin similar to ccRCC, tRCCs display distinct oncogenic programs and an immunosuppressive tumor microenvironment (TME). tRCCs exhibit six conserved tumor meta-programs, including epithelial-mesenchymal transition (EMT) and proximal tubule identity programs whose balance is regulated by TFE3 fusion activity. The fusion-driven EMT program drives a suppressive TME marked by progenitor-exhausted CD8 + T cells, anti-inflammatory SPP1+ macrophages, and matrix-associated fibroblasts. Our findings highlight unique TFE3 fusion-driven biology in tRCC, explaining its reduced immunotherapy responsiveness relative to ccRCC, and suggesting strategies for targeting fusion-driven oncogenic programs and TME reprogramming. - Source: PubMed
Publication date: 2026/08/26
Konda PrathyushaWakolbinger Alexandra JCui YantongRoberti de Oliveira GabrielNabil Yasmin LWeiss Cary NSeager Maxwell DDeodhar RivaLi JiaoMatar SayedWang JinyuHorst JackCamp Sabrina YSheshdeh Aseman BHecht Jonathan LEinstein David JRustagi YashikaNag AnweshaThorner Aaron RZhang Cheng-ZhongVan Allen Eliezer MSignoretti SabinaChoueiri Toni KViswanathan Srinivas R