Anti_Rat, pab VEGF_D Source Rabbit
- Known as:
- Anti_Rat, pab VEGF_D Source Rabbit
- Catalog number:
- 104-PA12S
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Rat pab VEGF_D Source Rabbit
Related genes to: Anti_Rat, pab VEGF_D Source Rabbit
- Gene:
- VEGFD NIH gene
- Name:
- vascular endothelial growth factor D
- Previous symbol:
- FIGF
- Synonyms:
- VEGF-D
- Chromosome:
- Xp22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-27
- Date modifiied:
- 2016-10-05
Related products to: Anti_Rat, pab VEGF_D Source Rabbit
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) 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"α - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS: Related articles to: Anti_Rat, pab VEGF_D Source Rabbit
- Diffuse cystic lung diseases (DCLDs) are a heterogeneous group of disorders requiring careful evaluation due to distinct management and prognostic implications. A 32-year-old woman presented with dyspnea and chest pressure following a coughing episode and was found to have a right-sided pneumothorax. CT chest showed bilateral, small, round-elliptiform, basal-predominant cysts. Workup, including autoimmune serologies and abdominal imaging, was unrevealing. Serum vascular endothelial growth factor (VEGF)-D was elevated at 839pg/ml, supporting a clinical diagnosis of lymphangioleiomyomatosis (LAM). However, critical re-evaluation of cyst morphology was more suggestive of Birt-Hogg-Dubé syndrome (BHD). Genetic testing revealed a pathogenic folluculin gene mutation, thus confirming the diagnosis of BHD. Surgical lung biopsy, obtained afterwards at the time of elective pleurodesis, did not reveal features of LAM. This case represents a rare instance of falsely elevated VEGF-D in patient with non-LAM DCLD and highlights the importance of critical review of chest radiology in the diagnostic evaluation of patients with cystic lung disease. - Source: PubMed
Publication date: 2026/06/07
Saluja PrachiShore Sarah KLombard Charles MRuoss Stephen JGupta Nishant - Blood group antigens are well known for their importance in transfusion medicine and transplant compatibility; however, their biological role extends beyond these functions and includes associations with the risk of several diseases. In this study, we investigated the relationship between ABO blood groups and the circulating levels of 73 different molecules. - Source: PubMed
Publication date: 2026/06/19
Di Salvo AlessiaMotisi ChiaraBulati MatteoScola LetiziaBalistreri Carmela Rita - Sirolimus is the standard disease-modifying therapy for lymphangioleiomyomatosis (LAM), but long-term routine-care data integrating pulmonary, lymphatic, extrapulmonary, and biomarker outcomes remain limited. - Source: PubMed
Publication date: 2026/06/12
Nowacka-Ejsmont JoannaBączek KarolBestry IwonaBłasinska KatarzynaSkronska PaulinaRozy AdrianaLangfort RenataSobiecka MałgorzataPujana Miquel AChorostowska-Wynimko JoannaMiłkowska-Dymanowska JoannaRadzikowska Elżbieta - Tuberous sclerosis complex (TSC) and Lymphangioleiomyomatosis (LAM) lack well-defined cellular origins, limiting treatment options. In this report, scRNA-seq of Tsc2+/- mouse renal cystadenomas revealed an 80-fold increase in a tumor cell subpopulation with neural crest features, and expressing known cranial neural crest genes as SRY box transcription factor 9 (Sox9), transcription factor activator protein (Tfap2a), and candidate neurocristopathy markers, osteopontin (Spp1), lipocalin-2 (Lcn2), clusterin (Clu), and cytokeratin 18 (Krt18). These signatures were validated in mouse tumors, and LAM patient lesions and serum, identifying a tumor phenotype distinct from traditional VEGFD detection. Pathway analysis indicated activation of WNT/SHH signaling, nephric duct formation, and pro-tumorigenic signals, with transcription factor 7 (Tcf7) and ephrin-A ligands as key upstream regulators. Spp1 KO in cranial neural crest cells (CNCCs) significantly reduced proliferation (28-33%), migration (54-76%), and invasion (29-64%) without affecting viability, while Tsc2 KO increased viability 3 to 6-fold with minimal impact on chemotaxis. Elevated serum levels of SPP1 and KRT18 in some LAM patients, decreased LCN2 in nearly all, and distinct increases in VEGFD suggest complementary roles for these biomarkers. Overall, findings support a neurocristopathic model of tumor development in TSC and LAM and identify potential biomarkers and therapeutic targets beyond mTOR inhibition. - Source: PubMed
Publication date: 2026/06/02
Unachukwu Uchenna JGarcia Enio BRai NooralamD'Armiento Jeanine M - Lymphangioleiomyomatosis (LAM) is a rare systemic disease characterized by cystic lung destruction, renal angiomyolipomas (AMLs), and lymphangioleiomyomas. It is classified into tuberous sclerosis complex-associated LAM (TSC-LAM) and sporadic LAM based on the TSC mutations. We reported monozygotic twin sisters of TSC-LAM with sirolimus therapy for ten years. Both twins presented cystic lung involvement, renal AMLs, cerebral MRI alterations, and severe ventilatory impairment at baseline. During long-term treatment, lung function remained stable in both patients, although exercise capacity declined. Despite identical genetics, clinically relevant differences were observed: one twin exhibited earlier disease onset, irregular menstruation, higher VEGF-D and poorer exercise tolerance at baseline. During treatment, she experienced greater weight loss, fluctuating sirolimus concentrations, and earlier need for oxygen therapy. These findings highlight substantial phenotypic heterogeneity in TSC-LAM despite shared genetics and emphasize the importance of early diagnosis, individualized management, and therapeutic drug monitoring in this complex disease. - Source: PubMed
Publication date: 2026/05/16
Fan LuElia DavideCassandro RobertoHarari Sergio Alfonso