SuperCult® Melanocyte Growth Medium Kit-4 is recommended media for melanocyte optimal growth and survival in culture. This medium is offered in our traditional Medium Kit format, providing flexibility to add or omit components as research needs dictate. ET-3 Growth Supplement, an additional growth factor required for adult melanocyte growth, is sold separately to supplement the Medium Kit for a complete formulation specifically designed for growing adult melanocytes. ET-3 offers enhanced growth and plating advantages in addition to limiting other cell type contamination in culture ...
Pharmacologic inhibition of bromodomain and extra-terminal (BET) proteins is currently being explored as a new therapeutic approach in cancer. Some studies have also implicated BET proteins as regulators of cell identity and differentiation through their interactions with lineage-specific factors. However, the role of BET proteins has not yet been investigated in melanocyte differentiation. Melanocyte inducing transcription factor (MITF) is the master regulator of melanocyte differentiation, essential for pigmentation and melanocyte survival. In this study, we tested the hypothesis that BET proteins regulate melanocyte differentiation through interactions with MITF. Here we show that chemical inhibition of BET proteins prevents differentiation of unpigmented melanoblasts into pigmented melanocytes and results in de-pigmentation of differentiated melanocytes. BET inhibition also slowed cell growth, without causing cell death, increasing the number of cells in G1. Transcriptional profiling revealed that
Pharmacologic inhibition of bromodomain and extra-terminal (BET) proteins is currently being explored as a new therapeutic approach in cancer. Some studies have also implicated BET proteins as regulators of cell identity and differentiation through their interactions with lineage-specific factors. However, the role of BET proteins has not yet been investigated in melanocyte differentiation. Melanocyte inducing transcription factor (MITF) is the master regulator of melanocyte differentiation, essential for pigmentation and melanocyte survival. In this study, we tested the hypothesis that BET proteins regulate melanocyte differentiation through interactions with MITF. Here we show that chemical inhibition of BET proteins prevents differentiation of unpigmented melanoblasts into pigmented melanocytes and results in de-pigmentation of differentiated melanocytes. BET inhibition also slowed cell growth, without causing cell death, increasing the number of cells in G1. Transcriptional profiling revealed that
Electron microscopic observations on normally differentiating and α-MSH (melanocytestimulating hormone)-treated epidermal melanocytes of newborn mouse skin were carried out. The process of melanocyte differentiation from premelanosome-containing melanoblasts was investigated in detail with respect to melanosomes as markers.. Melanoblasts containing unmelanized premelanosomes gradually decreased in number after birth, while the number of melanocytes rapidly increased. The epidermis of α-MSH-treated 3-day-old mice and normal 6-day-old mice contained melanocytes with numerous fully melanized melanosomes, and with no or only a few melanoblasts.. Changes in other organelles in differentiating melanocytes were also noticeable. Golgi apparatus and RER (rough endoplasmic reticulum) decreased in number during the normal or α-MSH-induced differentiation of the epidermal melanocytes, though the number of mitochondria showed no notable change. The number of SER (smooth endoplasmic reticulum) per cell did ...
Messenger RNA transcripts of the highly pigmented murine melanoma B16-F1 cells were compared with those from their weakly pigmented derivative B16-F10 cells by differential display. A novel gene called msg1 (melanocyte-specific gene) was found to be expressed at high levels in B16-F1 cells but at low levels in B16-F10 cells. Expression of msg1 was undetectable in the amelanotic K1735 murine melanoma cells. The pigmented murine melanocyte cell line melan-a expressed msg1, as did pigmented primary cultures of murine and human melanocytes; however, seven amelanotic or very weakly pigmented human melanoma cell lines were negative. Transformation of murine melanocytes by transfection with v-Ha-ras or Ela was accompanied by depigmentation and led to complete loss of msg1 expression. The normal tissue distribution of msg1 mRNA transcripts in adult mice was confined to melanocytes and testis. Murine msg1 and human MSG1 genes encode a predicted protein of 27 kDa with 75% overall amino acid identity and ...
In vitro studies have shown that the phorbol ester, 12-tetradecanoylphorbol 13-acetate (TPA) induces neural crest cell differentiation into melanocytes, and stimulates proliferation and differentiation of normal melanocytes. As TPA is not a physiological agent, its action is clearly mimicking some in vivo pathway involved in these processes. An understanding of the effect of TPA on the expression of melanogenic genes will therefore provide valuable insight into the molecular mechanisms regulating melanocyte differentiation. In this study, we utilized primary cultures of neural crest cells and an immortalized melanocyte cell line (DMEL-2) which proliferates in the absence of TPA, to explore the effects of TPA on key melanogenic effectors. In neural crest cells, TPA was found to be necessary for both microphthalmia associated transcription factor (Mitf) up-regulation and for melanin synthesis. Using northern blots, we show that in DMEL-2 cells, TPA significantly increases the messenger ribonucleic acid
Kim M.Y., Choi T.Y., Kim J.H., Lee J.H., Kim J.G., Sohn K.C., Yoon K.S., Kim C.D., Lee J.H., Yoon T.J.. BACKGROUND: Melanocyte dendrites serve as the principal conduit for melanosome transfer. The dendrite formation requires actin polymerization mediated by Rho family GTPases including RhoA, Rac1 and Cdc42. OBJECTIVE: The aim of this study is to investigate and explore the involvement of p38 MAPK in melanocyte dendrite formation. METHODS: We transduced melanoma cells with adenovirus harboring the expression cassette for constitutive active form of MKK6, an upstream MAPKK for p38 MAPK. RESULTS: We investigated the effect of melanogenic inducers on melanocyte dendricity, using SK-mel-24 melanoma cells because that this cell line is refractory to several melanogenic inducers in terms of melanogenesis. TPA-induced the phosphorylation of p38 MAPK and the elongation of dendrite length, suggesting that MKK6 may be involved in this process. Overexpression of the constitutive active form of MKK6 resulted ...
Tyrosinase-related protein 1, also known as TYRP1, is an enzyme which in humans is encoded by the TYRP1 gene. Tyrp1 is a melanocyte-specific gene product involved in melanin synthesis. While mouse Tyrp1 possesses dihydroxyindole carboxylic acid oxidase activity, the function in human melanocytes is less clear. In addition to its role in melanin synthesis, Tyrp1 is involved in stabilizing of tyrosinase protein and modulating its catalytic activity. Tyrp1 is also involved in maintenance of melanosome structure and affects melanocyte proliferation and melanocyte cell death. Mutations in the mouse Tyrp1 gene are associated with brown pelage and in the human TYRP1 gene with oculocutaneous albinism type 3 (OCA3). An allele of TYRP1 common in Solomon Islanders results in blond hair. Although the phenotype is similar to Northern European blond hair, this allele is not found in Europeans. The expression of TYRP1 is regulated by the microphthalmia-associated transcription factor (MITF). TYRP1 has been ...
McGill G.G., Horstmann M., Widlund H.R., Du J., Motyckova G., Nishimura E.K., Lin Y.L., Ramaswamy S., Avery W., Ding H.F., Jordan S.A., Jackson I.J., Korsmeyer S.J., Golub T.R., Fisher D.E.. Kit/SCF signaling and Mitf-dependent transcription are both essential for melanocyte development and pigmentation. To identify Mitf-dependent Kit transcriptional targets in primary melanocytes, microarray studies were undertaken. Among identified targets was BCL2, whose germline deletion produces melanocyte loss and which exhibited phenotypic synergy with Mitf in mice. BCL2s regulation by Mitf was verified in melanocytes and melanoma cells and by chromatin immunoprecipitation of the BCL2 promoter. Mitf also regulates BCL2 in osteoclasts, and both Mitf(mi/mi) and Bcl2(-/-) mice exhibit severe osteopetrosis. Disruption of Mitf in melanocytes or melanoma triggered profound apoptosis susceptible to rescue by BCL2 overexpression. Clinically, primary human melanoma expression microarrays revealed tight nearest ...
TY - JOUR. T1 - Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viability. AU - McGill, Gaël G.. AU - Horstmann, Martin. AU - Widlund, Hans R.. AU - Du, Jinyan. AU - Motyckova, Gabriela. AU - Nishimura, Emi K.. AU - Lin, Yi Ling. AU - Ramaswamy, Sridhar. AU - Avery, William. AU - Ding, Han Fei. AU - Jordan, Siobhán A.. AU - Jackson, Ian J.. AU - Korsmeyer, Stanley J.. AU - Golub, Todd R.. AU - Fisher, David E.. PY - 2002/6/14. Y1 - 2002/6/14. N2 - Kit/SCF signaling and Mitf-dependent transcription are both essential for melanocyte development and pigmentation. To identify Mitf-dependent Kit transcriptional targets in primary melanocytes, microarray studies were undertaken. Among identified targets was BCL2, whose germline deletion produces melanocyte loss and which exhibited phenotypic synergy with Mitf in mice. BCL2s regulation by Mitf was verified in melanocytes and melanoma cells and by chromatin immunoprecipitation of the BCL2 promoter. ...
The anaphase-promoting complex or cyclosome with the subunit Cdh1 (APC/CCdh1) is an E3 ubiquitin ligase involved in the control of the cell cycle. Here, we identified sporadic mutations occurring in the genes encoding APC components, including Cdh1, in human melanoma samples and found that loss of APC/CCdh1 may promote melanoma development and progression, but not by affecting cell cycle regulatory targets of APC/C. Most of the mutations we found in CDH1 were those associated with ultraviolet light (UV)-induced melanomagenesis. Compared with normal human skin tissue and human or mouse melanocytes, the abundance of Cdh1 was decreased and that of the transcription factor PAX3 was increased in human melanoma tissue and human or mouse melanoma cell lines, respectively; Cdh1 abundance was further decreased with advanced stages of human melanoma. PAX3 was a substrate of APC/CCdh1 in melanocytes, and APC/CCdh1-mediated ubiquitylation marked PAX3 for proteolytic degradation in a manner dependent on the ...
Cells and antibodies. The melanoma lines 624mel 526mel, C8161 (HAG) and C81-61 (PAG), SKmel2, SKmel24, MalMe3M, G361, WN115, MeWo, A375, WM266-4, HEK293T cell lines (ATCC), normal human epidermal melanocytes (PromoCell) and normal melanocyte cultures hmel-p-16, Nohm-4 and Hermes-2B were maintained as previously described (22, 59-61). The 34 primary cultures derived from surgically removed metastatic melanoma specimens were established and cultured as described (59). Stably transfected cell lines were cultured with 1 μg/ml puromycin (Calbiochem) or 2 mg/ml G418 (Alexis Biochemicals) The following primary antibodies were used: PE-His (Miltenyi Biotec), annexin V-FITC (Bender Medsystems), Ki67 (DAKO), ADAR1 (Sigma-Aldrich), β-actin (MP Biochemicals), Dicer (Abcam), Drosha (Abcam), DGCR8 (Abcam), and HRP-conjugated secondary antibodies (Jackson Immunoresearch).. RNA isolation and real-time qPCR analysis. Total RNA was isolated with Tri Reagent (Sigma-Aldrich) according to the manufacturers ...
Anti Human Melanocyte Cell Surface Antigen Antibody, clone 3C3 (Mel.2) , Mouse Anti-Human Monoclonal Antibody validated in IHC-F, IF, E (ABD13241), Abgent
The aggressive clinical behavior of melanoma suggests that the developmental origins of melanocytes in the neural crest might be relevant to their metastatic propensity. Here we show that primary human melanocytes, transformed using a specific set of introduced genes, form melanomas that frequently …
Ultraviolet (UV) radiation activates cell signaling pathways in melanocytes. As a result of altered signaling pathways and UV-induced cellular damage, melanocytes can undergo oncogenesis and develop into melanomas. In this study, we investigated the effect of UV-radiation on p38 MAPK (mitogen-activated protein kinase), JNK and NFκB pathways to determine which plays a major role in stimulating TNFα secretion in human HEM (melanocytes) and MM96L (melanoma) cells. MM96L cells exhibited 3.5-fold higher p38 activity than HEM cells at 5 min following UVA + B radiation and 1.6-fold higher JNK activity at 15-30 min following UVB+A radiation, while NFκB was minimally activated in both cells. Irradiated HEM cells had the greatest fold of TNFα secretion (UVB: 109-fold, UVA + B: 103-fold & UVB+A: 130-fold) when co-exposed to IL1α. The p38 inhibitor, SB202190, inhibited TNFα release by 93% from UVB-irradiated HEM cells. In the UVB-irradiated MM96L cells, both SB202190 and sulfasalazine (NFκB inhibitor)
a structure in the body that is composed of different kinds of tissue . Melanocytes are branched, or dendritic, and their dendrites are used to transfer pigment granules to adjacent epidermal cells. Certain melanocortins have been shown in laboratory testing to have effect on appetite and sexual activity in mice. This is mainly a consequence of alpha-MSH being secreted along with the hormone associated with reproductive tendencies in primates. But in some cases, changes to melanocytes can cause melanoma skin cancer. Organ. Our editors will review what youve submitted and determine whether to revise the article. [18], In addition to presenting antigen, one of the roles of melanocytes in the immune response is cytokine production. Albinism is often but not always related to the TYR gene coding the tyrosinase enzyme. Functionally, melanin serves as protection against UV radiation. Once synthesized, melanin is contained in special organelles called melanosomes which can be transported to nearby ...
Epidermal melanocytes highly pigmented, cryopreserved, not exposed to phenol red or antimicrobials. Optimized media kit especially for melanocytes.
Epidermal melanocytes highly pigmented, cryopreserved, not exposed to phenol red or antimicrobials. Optimized media kit especially for melanocytes.
The establishment of a single cell type regeneration paradigm in the zebrafish provides an opportunity to investigate the genetic mechanisms specific to regeneration processes. We previously demonstrated that regeneration melanocytes arise from cell division of the otherwise quiescent melanocyte precursors following larval melanocyte ablation with a small molecule, MoTP. The ease of ablating melanocytes by MoTP allows us to conduct a forward genetic screen for mechanisms specific to regeneration from such precursors or stem cells. Here, we reported the identification of two mutants, eartha(j23e1) and julie(j24e1) from a melanocyte ablation screen. Both mutants develop normal larval melanocytes, but upon melanocyte ablation, each mutation results in a distinct stage-specific defect in melanocyte regeneration. Positional cloning reveals that the eartha(j23e1) mutation is a nonsense mutation in gfpt1 (glutamine:fructose-6-phosphate aminotransferase 1), the rate-limiting enzyme in ...
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Epithelial cells constitute a protective barrier against the environment, but also serve as exchange interfaces with the outside world. To fulfill these functions, epithelial cells have evolved characteristic apical and basolateral plasma membrane regions. The basolateral membrane contacts neighboring cells and underlying tissue, whereas the apical membrane generally faces the lumen of an internal organ (Schuck and Simons, 2004). Melanocytes are epithelial cells that provide a first defense against solar exposure by distributing their pigment to overlying keratinocytes, and by communicating with other epithelial cells in the epidermis (Hearing, 2000). Melanocytes possess two functionally distinct types of cell surface: dendrites that are involved in the transfer of melanosomes to neighboring keratinocytes, and a central perinuclear region that is probably involved in cell-to-cell recognition. Owing to the similarities between polarized epithelial cells and melanocytes, we evaluated the ...
Normal melanocytes are found in the basal layer of the epidermis - the bottom part of the outer layer of the skin. The melanocytes produce a protein called melanin, which protects the skin by absorbing ultra violet (UV) radiation. Melanocytes are found in equal numbers in dark and white skin types but the melanocytes in dark skin produce much more melanin. People with dark brown or black skin are very much less likely to be damaged by UV radiation than those with white skin.. Non-cancerous growth of melanocytes causes common lesions like freckles and moles, whereas cancerous growth causes melanoma. There are different types of melanoma and if picked up early enough, melanoma can be cured.. ...
During melanocyte development, the cytokine Steel factor activates its receptor c-Kit, initiating a signal transduction cascade, which is vital for lineage determination via unknown downstream nuclear targets. c-Kit has recently been found to trigger mitogen-activated protein kinase-mediated phosphorylation of Microphthalmia (Mi), a lineage- restricted transcription factor, which, like Steel factor and c-Kit, is essential for melanocyte development. This cascade results in increased Mi-dependent transcriptional reporter activity. Here we examine the mechanism by which Mi is activated by this pathway. Phosphorylation does not significantly alter Mis nuclear localization, DNA binding, or dimerization. However, the transcriptional coactivator p300/CBP selectively associates with mitogen-activated protein kinase- phosphorylated Mi, even under conditions in which non-MAPK phospho-Mi is more abundant. Moreover, p300/CBP coactivates Mi transcriptional activity in a manner dependent upon this phosphorylation.
Pull out of epidermis in a cut-away model of the skin, dissolve on melanocytes. Melanocytes manufacture the pigment melanin, which helps filter dangerous ultraviolet, or uv. rays that can cause wrinkles and skin cancer. - Stock Video Clip K005/0014
A prospective open-label, randomized, multicenter clinical trial was conducted with 22 patients. Each subject was treated with cultured graft and polyurethane dressing (control arm) after epidermal ablation and followed for up to 9 months. The extent of repigmentation in the treated sites was compared with that control sites at days 90, 180, and 270. ...
A close contact between melanocytes and nerve fibers in the epidermis has been demonstrated in normal human skin. The interactions between the neural and immune systems play an important role in the pathophysiology of certain dermatoses. In this study, we investigated the intraepidermal nerve fibers and their contacts with melanocytes in the lesions of melasma…
Skin: Epidermis - Melanocytes Melanocytes: Melanocytes: -In stratum basale -Pale halo of cytoplasm -Neural crest -Produce melanin and pass it on to nearby keratinocytes -Melanin covers nuclei of nearby keratinocytes -Skin colour depends on melanocytes activity, rather than the number present
The TRPM family proteins have a wide range of physiological functions that include sensing taste, ambient temperature, and osmolarity (16). It is, therefore, of interest to note that melanocytes, which are thought to respond to physiological and environmental stimuli, show expression of TRPMs 1, 3, 4, 6, and 7 mRNAs, suggesting that multiple TRPM genes are transcribed in melanocytes and may be involved in melanocyte function and skin pigmentation. For example, TRPM 7, the cation-permeable channel and key regulator of Mg+2 homeostasis, has recently been shown to be involved in detoxification of melanin synthesis intermediates in zebrafish melanophores and also expressed in human melanoma cells (23).. Although TRPM1, the founding member of the TRPM family, was identified as melanocyte-selective protein, the functions of this protein are not known. Our data show that TRPM1 acts as an active Ca2+ channel in melanocytes. Calcium is involved in a wide range of vital cell functions including cell ...
Olfactory receptor. The activity of this receptor is propably mediated by G-proteins wich induce elevation of intracellular Ca(2+), cAMP and activation of phosphorylation of the protein kinases PKA and MAPK3/MAPK1. Activation of OR51E2 may affect melanocyte proliferation, differentiation, and melanogenesis and may increase proliferation and migration of primary retinal pigment epithelial (RPE) cells (By similarity). Activated by the short chain fatty acids (SCFA), acetate and propionate (PubMed:23401498). In response to SCFA, may positively regulate renin secretion and increase blood pressure (PubMed:23401498). May also be activated by steroid hormones and regulate cell proliferation (By similarity). Activated by L-lactate in glomus cells (PubMed:26560302, PubMed:30258151).
Oral Malignant Melanoma in Dogs and Cats Melanoma is a tumor of melanocytes, which arise from neural crest cells and function to synthesize melanin. Melanocytes are commonly located in the oral cavity, haired skin and eye, making these the most common locations where melanomas arise. Biologic behavior of melanoma depends in part on tumor location. The majority of melanomas that arise in the oral cavity are classified both histologically and biologically as malignant. Histologic features that support a diagnosis of oral malignant melanoma include a mitotic index greater than 2 mitoses per 10 high-powered fields, nuclear atypia, vascular or lymphatic invasion and ulceration. Malignant tumors may be variably pigmented or amelanotic (one third of cases). Since melanocytes are derived from neural crest cells, which ultimately give rise to both glandular tissues and connective tissues, melanomas can resemble both carcinomas and sarcomas morphologically. Given these challenges to diagnosing a malignant ...
Helpful, trusted answers from doctors: Dr. Wingo on melanocyte stimulating hormone: It's hard to say which one stimulates which; oftentimes multiple factors are interacting to make a organ properly function although one of the involved factors may play a major role for its overall functions. For sperm formation, FSH (follicule-stimulating hormone) is the key one but conjuncting with healthy testicular tissue and LH as well as testosterone. More? Ask your Dr., preferably urologist
Randerson-Moor et al., 2001). Furthermore, Sviderskaya et al. (2002) reported that the expression of Ink4a-Arf in mice causes melanocyte senescence and stimulates pigment synthesis. A plausible mechanism for Sex-linked barring in chickens is that the CDKN2A mutation(s) we identified results in premature cell death, which in turn leads to the formation of white bars lacking melanocytes. This may then be followed by a new wave of melanocytes recruited from a pool of stem cells, which migrate, colonize the feather follicle, produce melanin and form the next black bar ...
Moles are reason by the melanocyte cells in the skin. Melanocyte cells make melanin and are conscientious for the color of the skin, hair and eyes. They are sha
The development of a modified stromal microenvironment in response to neoplastic onset is a common feature of many tumors including cutaneous melanoma. At all stages, melanoma cells are embedded in a complex tissue composed by extracellular matrix components and several different cell populations. Thus, melanomagenesis is not only driven by malignant melanocytes, but also by the altered communication between melanocytes and non-malignant cell populations, including fibroblasts, endothelial and immune cells. In particular, cancer-associated fibroblasts (CAFs), also referred as melanoma-associated fibroblasts (MAFs) in the case of melanoma, are the most abundant stromal cells and play a significant contextual role in melanoma initiation, progression and metastasis. As a result of dynamic intercellular molecular dialogue between tumor and the stroma, non-neoplastic cells gain specific phenotypes and functions that are pro-tumorigenic. Targeting MAFs is thus considered a promising avenue to improve melanoma
Circular RNAs (circRNAs) play critical roles in the occurrence of human diseases, including cancer. However, the detailed functions of circRNAs in melanoma have not been fully elucidated. In the present study, a circRNA microarray was performed to analyze the variability of circRNAs in the low-metastatic melanoma WM35 cell line and in the high-metastatic melanoma WM451 cell line in comparison to control human melanocytes. The results revealed that five circRNAs were upregulated and four circRNAs were downregulated in both the WM35 and WM451 cells. qRT-PCR revealed an upregulated expression of circ0000082 and circ0016418 and a downregulation of circ0023988, circ0008157 and circ0030388 in the cells which was consistent with the results of the microarray assay. Functional tests revealed that knockdown of circ0023988, circ0008157 or circ0030388 significantly promoted the proliferation and invasion of the WM35 cells. Following the silencing of circ0000082 or circ0016418 in WM451 cells, the ...
Genomic profiling technology has identified purported driver mutations in various cancers, but it is most often the proteins that drive tumor development and present therapeutic targets. Furthermore, tumor genomic profiling misses the contribution of cells of the tumor microenvironment to tumor progression. Using multiepitope ligand cartography on human skin samples, Ostalecki et al. identified changes in protein abundance and subcellular localization in melanocytes and keratinocytes that were associated with various stages of melanoma development. The findings revealed the transfer of a peptidase-metalloproteinase pair from early-stage BRAF-mutant/PTEN-null melanoma cells to adjacent normal keratinocytes through cell contact. The recipient keratinocytes exhibited altered protein abundance and secretion. Inhibiting this intercellular mode of communication and its effects might be therapeutic in melanoma patients. ...
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BRAF drives tumorigenesis by coordinating the activation of the RAS/RAF/MEK/ERK oncogenic signaling cascade. However, upstream pathways governing BRAF kinase activity and protein stability remain undefined. Here, we report that in primary cells with active APCFZR1, APCFZR1 earmarks BRAF for ubiquitination-mediated proteolysis, whereas in cancer cells with APC-free FZR1, FZR1 suppresses BRAF through disrupting BRAF dimerization. Moreover, we identified FZR1 as a direct target of ERK and CYCLIN D1/CDK4 kinases. Phosphorylation of FZR1 inhibits APCFZR1, leading to elevation of a cohort of oncogenic APCFZR1 substrates to facilitate melanomagenesis. Importantly, CDK4 and/or BRAF/MEK inhibitors restore APCFZR1 E3 ligase activity, which might be critical for their clinical effects. Furthermore, FZR1 depletion cooperates with AKT hyperactivation to transform primary melanocytes, whereas genetic ablation of Fzr1 synergizes with Pten loss, leading to aberrant coactivation of BRAF/ERK and AKT signaling in ...
Melanoma is a cancer of the skin which develops from the cell which produces our skin colour or pigment. That cell is the melanocyte. The melanocyte sits within the scaly top layer of the skin (the epidermis) manufacturing pigment and injecting the pigment into the nearby skin cells (keratinocytes). The number of melanocytes that we all have is pretty similar but humans vary in the type of pigment produced and how that pigment is distributed in the skin cells. The nature and distribution of the pigment determines our skin colour and how vulnerable the skin is to sun burn. This is important as the evidence is that sunburn and damage resulting from burning is what leads to genetic changes (mutations) in the melanocytes which ultimately lead to the development of melanomas.. Epidemiological research has shown that melanoma has become steadily more common in pale skinned populations since the early part of the 20th century but the increase in the last 10 years has been especially dramatic and ...
Transcription factors are central players in the regulatory networks that control differentiation in all types of precursor cells and stem cells. Itis well know...
Fingerprint Dive into the research topics of Differentially expressed circRNAs in melanocytes and melanoma cells and their effect on cell proliferation and invasion. Together they form a unique fingerprint. ...
Benign lesions exist in a stable antiproliferative state due to activation of oncogene-induced senescence (OIS), which must be bypassed in order for full malignant transformation to occur. The oncogenic BRAFV600E mutation has been found in both growth-arrested melanocytic nevi and melanomas, suggesting that additional genetic alterations are required for melanomagenesis. Although CDKN2A and PI3K-AKT signaling have been implicated in mediating OIS bypass in melanoma, the specific factors required for progression remain unclear. Damsky and colleagues generated multiple melanocyte-specific BrafV600E mouse models and found that inactivation of Cdkn2a in the context of BrafV600E led to growth-arrested nevi that stochastically progressed to melanoma at a rate similar to that observed in humans. Characterization of gene expression profiles from pre-arrest melanocytes, growth-arrested melanocytes, and melanomas from Cdkn2a/BrafV600E mice revealed downregulation of mTOR signaling upon growth arrest and ...
Adenosine 3,5-monophosphate (cyclic AMP) as the mediator of the actions of melanocyte stimulating hormone (MSH) and norepinephrine on the frog skin.
Melanocyte, definition and possible consequences on Childrens skin and the sun thanks to La Roche-Posay, the brand recommended by over 25,000 dermatologists
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Sigma-Aldrich offers Sigma-M8267, des-Ac-α-Melanocyte Stimulating Hormone for your research needs. Find product specific information including CAS, MSDS, protocols and references.
Melanocyte, definition and possible consequences on Sun For Everyone thanks to La Roche-Posay, the brand recommended by over 25,000 dermatologists
1 Mb copy number variant (CNV) harboring 5 genes including EDNRA ; The duplicated EDNRA copies contain a missense variant (p.Tyr129His) predicted to increase the affinity of the encoded mutant receptor for endothelin 3. Menzi et al. proposed a hypothesis whereby ectopic overexpression of a mutant EDNRA scavenges EDN3 required for EDNRB signaling and normal melanocyte development and thus likely leads to an absence of melanocytes in the non-pigmented body areas of Boer goats (thanks to OMIA for the summary ...
3762 In its normal life cycle, B. pertussis attaches to, and invades ciliated epithelia and macrophages of the human airways, using adhesins specialized for certain oligosaccharides and proteins on these cells. Here we report that B. pertussis uses similar mechanisms for invasion of a variety of human cancer cells in vitro, and exhibits potent, invasion-dependent, cytotoxicity. In a 30′ in vitro invasion assay, B. pertussis invaded human SKmel-23 melanoma cells at 20-30 times the rate for normal human melanocytes and fibroblasts. B. pertussis invasion of SKmel-23 cells was inhibited by preincubation of cancer cells with glycosidase F, the plant lectins LPHA and TGP, human antibodies vs CD15 and CD11b, or the RGD tripeptide sequence-implying that the structural requirements for invasion included β1,6-branched N-glycans, Lewis × antigens, CD11b, and the sequence arg-gly-asp respectivelly. Invasion was also inhibited by preincubation of cancer cells with 3-methyladenine (3-MA), indicating a ...
Craig J. Ceol, PhD, is using the zebrafish to study melanoma, the most deadly form of skin cancer, and melanocytes, the pigment-producing cells in human skin that can become cancerous melanoma. Over the last 40 years, melanoma rates have increased more than 200 percent, and melanoma is now the most common form of cancer in adults between the ages of 25 and 29.